Acute Respiratory Distress Syndrome https://greenmedinfo.com/taxonomy/term/520/all en Acute respiratory distress syndrome: Predictors of noninvasive ventilation failure and intensive care unit mortality in clinical practice. https://greenmedinfo.com/article/acute-respiratory-distress-syndrome-predictors-noninvasive-ventilation-failure PMID:  J Crit Care. 2016 Feb ;31(1):26-30. Epub 2015 Oct 30. PMID: 26643859 Abstract Title:  Acute respiratory distress syndrome: Predictors of noninvasive ventilation failure and intensive care unit mortality in clinical practice. Abstract:  PURPOSE: Noninvasive ventilation (NIV) is used as an initial ventilatory support in acute respiratory distress syndrome (ARDS), but its utility is unclear, and persistence in those who do not improve may delay intubation and lead to adverse outcomes. Hence, it becomes imperative to have a clear understanding of selecting patients who will benefit from this modality.METHODS: In this prospective observational study, we included all consecutive adults, over a 3-year period, who fulfilled criteria for ARDS by the Berlin definition. Basic demographics, ventilatory support, intensive care unit course, and outcome were recorded.RESULTS: Of 170 patients, 96 (56.47%) were initially managed with NIV. Noninvasive ventilation failure was seen in 42 (43.75%) of 96, and low baseline PaO2/FIO2, shock, and ARDS severity were associated with NIV failure. Overall intensive care unit mortality was 63 (37.1%) of 170, and high Acute Physiology and Chronic Health Evaluation II score, low PaO2/FIO2, shock, and ARDS severity were associated with increased mortality. Noninvasive ventilation failure and mortality were significantly higher in moderate and severe ARDS.CONCLUSIONS: Noninvasive ventilation maybe useful in selected patients with mild ARDS but should be used with great caution in moderate and severe ARDS, as failure risk is high. In addition, low PaO2/FIO2 and shock are associated with NIV failure. Acute Physiology and Chronic Health Evaluation II score, shock, low PaO2/FIO2, and ARDS severity are associated with increased mortality. <p><a href="https://greenmedinfo.com/article/acute-respiratory-distress-syndrome-predictors-noninvasive-ventilation-failure" target="_blank">read more</a></p> https://greenmedinfo.com/article/acute-respiratory-distress-syndrome-predictors-noninvasive-ventilation-failure#comments Acute Respiratory Distress Syndrome Increased Risk Pneumonia: Ventilator-associated Human Study Thu, 09 Apr 2020 22:52:46 +0000 greenmedinfo 218299 at https://greenmedinfo.com Andrographolide is worth to be clinically further studied in ARDS treatment. https://greenmedinfo.com/article/andrographolide-worth-be-clinically-further-studied-ards-treatment PMID:  Intensive Care Res. 2022 ;2(3-4):61-70. Epub 2022 Jul 13. PMID: 36523372 Abstract Title:  Andrographolide Suppresses Expressions of Coagulation and Fibrinolytic Inhibition-Related Factors in LPS-Induced Alveolar Epithelial Cell Type II via NF-κB Signal Pathway In Vitro. Abstract:  BACKGROUND: Andrographolide (Andro) has been confirmed to ameliorate alveolar hypercoagulation and fibrinolysis inhibition via NF-κB pathway in acute respiratory distress syndrome (ARDS), but the specific target of Andro is unknown.PURPOSE: Our aim is to explore the specific target of Andro through which the drug exerted its effects on alveolar hypercoagulation and fibrinolytic inhibition in LPS-induced ARDS.METHODS: AECII was treated with different doses of Andro for 1 h, and then stimulated with LPS for 24 h. Expressions of tissue factor (TF), plasminogen activator inhibitor (PAI)-1 and tissue factor pathway inhibitor (TFPI) were detected. Concentrations of thrombin-antithrombin complex (TAT), pro-collagen type III peptide (PIIIP), antithrombin III (ATIII) and activated protein C (APC) in cell supernatant were measured by enzyme linked immunosorbent assay (ELISA). NF-κB signaling pathways activation was simultaneously determined. AECII with p65 down-/over-expression were used as control.RESULTS: Andro effectively inhibited TF and PAI-1 and promoted TFPI expressions on AECII induced by LPS stimulation. Andro also significantly suppressed the productions of TAT and PIIIP but promoted ATIII and APC secretions from the LPS-treated cell. Furthermore, Andro application obviously inhibited NF-κB signaling pathway activation provoked by LPS, as shown by decreased level of phosphorylation (p‑)-IKKβ/IKKβ, p-p65/p65 and p65 DNA binding activity. The effects of Andro on those factors were obviously strengthened by down- but were weakened by up-regulation of p65 gene in AECII cell.CONCLUSIONS: Our data demonstrates that targeting AECII is the mechanism by which Andro ameliorates alveolar hypercoagulaiton and fibrinolytic inhibition via NF-κB pathway in ARDS. Andro is worth to be clinically further studied in ARDS treatment. <p><a href="https://greenmedinfo.com/article/andrographolide-worth-be-clinically-further-studied-ards-treatment" target="_blank">read more</a></p> https://greenmedinfo.com/article/andrographolide-worth-be-clinically-further-studied-ards-treatment#comments Acute Respiratory Distress Syndrome Andrographolide Anti-Inflammatory Agents NF-kappaB Inhibitor In Vitro Study Wed, 28 Dec 2022 22:06:09 +0000 greenmedinfo 268582 at https://greenmedinfo.com Astragaloside IV attenuates lipopolysaccharides-induced pulmonary epithelial cell injury through inhibiting autophagy. https://greenmedinfo.com/article/astragaloside-iv-attenuates-lipopolysaccharides-induced-pulmonary-epithelial-c PMID:  Pharmacology. 2019 Sep 25:1-12. Epub 2019 Sep 25. PMID: 31554002 Abstract Title:  Astragaloside IV Attenuates Lipopolysaccharides-Induced Pulmonary Epithelial Cell Injury through Inhibiting Autophagy. Abstract:  BACKGROUND: Astragaloside IV has shown its promising effect on acute respiratory distress syndrome (ARDS).OBJECTIVES: We aim to explore whether astragaloside IV is effective for ARDS treatment in a lipopolysaccharides (LPS)-induced cell model and whether autophagy is involved in the therapeutic function of astragaloside IV.METHODS: MLE-12 cells were induced by LPS to construct an ARDS model in vitro. Cell viability was estimated by cell counting kit-8 and cell apoptosis by flow cytometry. Lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by enzyme-linked immunosorbent assay kit. The expression of tumour necrosis factor (TNF)-α, interleukin (IL)-6, zonula occludens (ZO)-1, Beclin-1 and autophagy-related (atg) 5 mRNA was evaluated by quantitative PCR, and the expression of ZO-1, microtubule-associated proteins 1A/1B light chain 3B (LC3B) I and, LC3B II protein by Western blot.RESULTS: LPS effectively inhibited cell viability and LC3B I expression and enhanced LC3B II, Beclin-1 and atg5 expressions in MLE-12 cells. In LPS-induced ARDS cell model, astragaloside IV up-regulated cell viability, SOD activity and ZO-1 and LC3B I expressions but down-regulated cell apoptosis, TNF-α, IL-6, LC3B II, Beclin-1 and atg5 expressions and LDH and MDA levels. 3-methyladenine promoted cell viability and ZO-1 expression, down-regulated Beclin-1 and atg5 expression, while Rapamycin (Rap) had an opposite effect. Astragaloside IV suppressed cell viability and ZO-1 expression after the Rap treatment.CONCLUSIONS: Astragaloside IV might suppress autophagy initiation directly or indirectly through suppressing the oxidative stress and inflammatory response, which further enhances the cell viability and tight junction and reduces apoptosis in LPS-stimulated pulmonary endothelial ARDS cell model, thus exerting its therapeutic function in ARDS. <p><a href="https://greenmedinfo.com/article/astragaloside-iv-attenuates-lipopolysaccharides-induced-pulmonary-epithelial-c" target="_blank">read more</a></p> https://greenmedinfo.com/article/astragaloside-iv-attenuates-lipopolysaccharides-induced-pulmonary-epithelial-c#comments Acute Respiratory Distress Syndrome Astragaloside Lipopolysaccharide-Induced Toxicity Anti-Inflammatory Agents Autophagy Inhibitors Interleukin-6 Downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor In Vitro Study Tue, 01 Oct 2019 22:52:40 +0000 greenmedinfo 197792 at https://greenmedinfo.com Berberine alleviates endothelial glycocalyx degradation and promotes glycocalyx restoration in LPS-induced ARDS. https://greenmedinfo.com/article/berberine-alleviates-endothelial-glycocalyx-degradation-and-promotes-glycocaly PMID:  Int Immunopharmacol. 2018 Oct 8 ;65:96-107. Epub 2018 Oct 8. PMID: 30308440 Abstract Title:  Berberine alleviates endothelial glycocalyx degradation and promotes glycocalyx restoration in LPS-induced ARDS. Abstract:  In the pathogenesis of acute respiratory distress syndrome (ARDS), an increase in vascular endothelial permeability may trigger pulmonary edema and ultimately lead to respiratory failure. Endothelial glycocalyx damage is an important factor that causes an increase in vascular endothelial permeability. Berberine (BBR) is an isoquinoline alkaloid extracted from Coptis chinensis, a plant used in traditional Chinese medicine that exerts multiple pharmacological effects. In this study, pretreatment with BBR inhibited the increase in vascular endothelial permeability in mice with lipopolysaccharide (LPS)-induced ARDS. BBR pretreatment inhibited the shedding of syndecan-1 (SDC-1) and heparan sulfate (HS), which are important components of the endothelial glycocalyx that lessen endothelial glycocalyx damage. BBR further significantly inhibited increases in important endothelial glycocalyx damage factors, including reactive oxygen species (ROS), heparanase (HPA), and matrix metalloproteinase 9 (MMP9) in LPS-induced ARDS mice and in LPS-stimulated human umbilical vein endothelial cells. BBR pretreatment also decreased the production of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and inhibited NF-κB signaling pathway activation in LPS-induced ARDS. In addition, BBR promoted the recovery of SDC-1 and HS content in injured endothelial glycocalyx after LPS treatment and accelerated its restoration. This is the first report of BBR maintaining the integrity ofendothelial glycocalyx. These results provide a new theoretical basis for the use of BBR in the treatment of ARDS and other diseases related to endothelial glycocalyx damage. <p><a href="https://greenmedinfo.com/article/berberine-alleviates-endothelial-glycocalyx-degradation-and-promotes-glycocaly" target="_blank">read more</a></p> https://greenmedinfo.com/article/berberine-alleviates-endothelial-glycocalyx-degradation-and-promotes-glycocaly#comments Acute Respiratory Distress Syndrome Berberine Lipopolysaccharide-Induced Toxicity Anti-Inflammatory Agents Interleukin-1 beta downregulation Interleukin-6 Downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Mon, 29 Oct 2018 20:55:59 +0000 greenmedinfo 173150 at https://greenmedinfo.com Carnosic acid inhibits reactive oxygen species-dependent neutrophil extracellular trap formation and ameliorates acute respiratory distress syndrome. https://greenmedinfo.com/article/carnosic-acid-inhibits-reactive-oxygen-species-dependent-neutrophil-extracellu PMID:  Life Sci. 2022 Dec 29:121334. Epub 2022 Dec 29. PMID: 36587789 Abstract Title:  Carnosic acid inhibits reactive oxygen species-dependent neutrophil extracellular trap formation and ameliorates acute respiratory distress syndrome. Abstract:  AIMS: Infiltration of activated neutrophils into the lungs is a hallmark of acute respiratory distress syndrome (ARDS). Neutrophilic inflammation, particularly neutrophil extracellular traps (NETs), is proposed as a useful target for treating ARDS. Carnosic acid (CA) is a food additive; however, its anti-neutrophilic activity in the treatment of ARDS has not been well established. The hypothesis of present study is to confirm that CA alleviates ARDS by suppressing neutrophilic inflammation and oxidative damage.MAIN METHODS: Generation of superoxide anions and reactive oxygen species (ROS), induction of elastase degranulation, and formation of NETs by human neutrophils were assayed using spectrophotometry, flow cytometry, and immunofluorescent microscopy. Immunoblotting was performed to determine the cellular mechanisms involved. Cell-free radical systems were used to test antioxidant activities. The therapeutic effect of CA was evaluated in a lipopolysaccharide (LPS)-induced ARDS mouse model.KEY FINDINGS: CA greatly reduced superoxide anion production, ROS production, elastase release, cluster of differentiation 11b expression, and cell adhesion in activated human neutrophils. Mechanistic studies have demonstrated that CA suppresses phosphorylation of extracellular regulated kinase and c-Jun N-terminal kinase in activated neutrophils. CA effectively scavenges reactive oxygen and nitrogen species, but not superoxide anions. This is consistent with the finding that CA is effective against ROS-dependent NET formation. CA treatment significantly improved pulmonary neutrophil infiltration, oxidative damage, NET formation, and alveolar damage in LPS-induced mice.SIGNIFICANCE: Our data suggested the potential application of CA for neutrophil-associated ARDS therapy. <p><a href="https://greenmedinfo.com/article/carnosic-acid-inhibits-reactive-oxygen-species-dependent-neutrophil-extracellu" target="_blank">read more</a></p> https://greenmedinfo.com/article/carnosic-acid-inhibits-reactive-oxygen-species-dependent-neutrophil-extracellu#comments Acute Respiratory Distress Syndrome Carnosic Acid Antioxidants Animal Study Sun, 08 Jan 2023 23:03:32 +0000 greenmedinfo 269168 at https://greenmedinfo.com Chlorogenic acid may be a viable therapeutic option for bacterial and viral-induced acute respiratory distress syndrome-like pathology. https://greenmedinfo.com/article/chlorogenic-acid-may-be-viable-therapeutic-option-bacterial-and-viral-induced- PMID:  Clin Sci (Lond). 2023 May 31 ;137(10):785-805. PMID: 36951146 Abstract Title:  Targeting TLR4/3 using chlorogenic acid ameliorates LPS+POLY I:C-induced acute respiratory distress syndrome via alleviating oxidative stress-mediated NLRP3/NF-κB axis. Abstract:  Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is a life-threatening condition caused due to significant pulmonary and systemic inflammation. Chlorogenic acid (CGA) has been shown to possess potent antioxidant, anti-inflammatory, and immunoprotective properties. However, the protective effect of CGA on viral and bacterial-induced ALI/ARDS is not yet explored. Hence, the current study is aimed to evaluate the preclinical efficacy of CGA in lipopolysaccharide (LPS) and polyinosinic:polycytidylic acid (POLY I:C)-induced ALI/ARDS models in vitro and in vivo. Human airway epithelial (BEAS-2B) cells exposed to LPS+POLY I:C significantly elevated oxidative stress and inflammatory signaling. Co-treatment with CGA (10 and 50µM) prevented inflammation and oxidative stress mediated by TLR4/TLR3 and NLRP3 inflammasome axis. BALB/c mice, when chronically challenged with LPS+POLY I:C showed a significant influx of immune cells, up-regulation of pro-inflammatory cytokines, namely: IL-6, IL-1β, and TNF-α, and treatment with intranasal CGA (1 and 5 mg/kg) normalized the elevated levels of immune cell infiltration as well as pro-inflammatory cytokines. D-Dimer, the serum marker for intravascular coagulation, was significantly increased in LPS+ POLY I:C challenged animals which was reduced with CGA treatment. Further, CGA treatment also has a beneficial effect on the lung and heart, as shown by improving lung physiological and cardiac functional parameters accompanied by the elevated antioxidant response and simultaneous reduction in tissue damage caused by LPS+POLY I:C co-infection. In summary, these comprehensive, in vitro and in vivo studies suggest that CGA may be a viable therapeutic option for bacterial and viral-induced ALI-ARDS-like pathology. <p><a href="https://greenmedinfo.com/article/chlorogenic-acid-may-be-viable-therapeutic-option-bacterial-and-viral-induced-" target="_blank">read more</a></p> https://greenmedinfo.com/article/chlorogenic-acid-may-be-viable-therapeutic-option-bacterial-and-viral-induced-#comments Acute Respiratory Distress Syndrome Chlorogenic Acid Inflammation Lipopolysaccharide-Induced Toxicity Oxidative Stress Anti-Inflammatory Agents Antioxidants Interleukin-1 beta downregulation Interleukin-6 Downregulation NF-kappaB Inhibitor Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study In Vitro Study Fri, 23 Jun 2023 19:27:28 +0000 greenmedinfo 275573 at https://greenmedinfo.com Clinical management of COVID-19 in cancer patients with the STAT3 inhibitor silibinin. https://greenmedinfo.com/article/clinical-management-covid-19-cancer-patients-stat3-inhibitor-silibinin PMID:  Pharmaceuticals (Basel). 2021 Dec 24 ;15(1). Epub 2021 Dec 24. PMID: 35056076 Abstract Title:  Clinical Management of COVID-19 in Cancer Patients with the STAT3 Inhibitor Silibinin. Abstract:  COVID-19 pathophysiology is caused by a cascade of respiratory and multiorgan failures arising, at least in part, from the SARS-CoV-2-driven dysregulation of the master transcriptional factor STAT3. Pharmacological correction of STAT3 over-stimulation, which is at the root of acute respiratory distress syndrome (ARDS) and coagulopathy/thrombosis events, should be considered for treatment of severe COVID-19. In this perspective, we first review the current body of knowledge on the role of STAT3 in the pathogenesis of severe COVID-19. We then exemplify the potential clinical value of treating COVID-19 disease with STAT3 inhibitors by presenting the outcomes of two hospitalized patients with active cancer and COVID-19 receiving oral Legalon-a nutraceutical containing the naturally occurring STAT3 inhibitor silibinin. Both patients, which were recruited to the clinical trial SIL-COVID19 (EudraCT number: 2020-001794-77) had SARS-CoV-2 bilateral interstitial pneumonia and a high COVID-GRAM score, and showed systemic proinflammatory responses in terms of lymphocytopenia and hypoalbuminemia. Both patients were predicted to be at high risk of critical COVID-19 illness in terms of intensive care unit admission, invasive ventilation, or death. In addition to physician&#039;s choice of best available therapy or supportive care, patients received 1050 mg/day Legalonfor 10 days without side-effects. Silibinin-treated cancer/COVID-19+ patients required only minimal oxygen support (2-4 L/min) during the episode, exhibited a sharp decline of the STAT3-regulated C-reactive protein, and demonstrated complete resolution of the pulmonary lesions. These findings might inspire future research to advance our knowledge and improve silibinin-based clinical interventions aimed to target STAT3-driven COVID-19 pathophysiology. <p><a href="https://greenmedinfo.com/article/clinical-management-covid-19-cancer-patients-stat3-inhibitor-silibinin" target="_blank">read more</a></p> https://greenmedinfo.com/article/clinical-management-covid-19-cancer-patients-stat3-inhibitor-silibinin#comments Acute Respiratory Distress Syndrome Coronavirus Infection Silibinin STAT3 Inhibitor Human Study Sat, 12 Mar 2022 21:53:02 +0000 greenmedinfo 254595 at https://greenmedinfo.com COVID-19: Melatonin as a potential adjuvant treatment. https://greenmedinfo.com/article/covid-19-melatonin-potential-adjuvant-treatment n/a PMID:  Life Sci. 2020 Mar 23:117583. Epub 2020 Mar 23. PMID: 32217117 Abstract Title:  COVID-19: Melatonin as a potential adjuvant treatment. Abstract:  This article summarizes the likely benefits of melatonin in the attenuation of COVID-19 based on its putative pathogenesis. The recent outbreak of COVID-19 has become a pandemic with tens of thousands of infected patients. Based on clinical features, pathology, the pathogenesis of acute respiratory disorder induced by either highly homogenous coronaviruses or other pathogens, the evidence suggests that excessive inflammation, oxidation, and an exaggerated immune response very likely contribute to COVID-19 pathology. This leads to a cytokine storm and subsequent progression to acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and often death. Melatonin, a well-known anti-inflammatory and anti-oxidative molecule, is protective against ALI/ARDS caused by viral and other pathogens. Melatonin is effective in critical care patients by reducing vessel permeability, anxiety, sedation use, and improving sleeping quality, which might also be beneficial for better clinical outcomes for COVID-19 patients. Notably, melatonin has a high safety profile. There is significant data showing that melatonin limits virus-related diseases and would also likely be beneficial in COVID-19 patients. Additional experiments and clinical studies are required to confirm this speculation. https://greenmedinfo.com/article/covid-19-melatonin-potential-adjuvant-treatment#comments Acute Respiratory Distress Syndrome Coronavirus Infection Lung Injury: Acute Melatonin Anti-Inflammatory Agents Antioxidants Immunomodulatory Cytokine Storm Review Fri, 03 Apr 2020 14:11:34 +0000 greenmedinfo 217848 at https://greenmedinfo.com Diosmetin alleviates lipopolysaccharide-induced acute lung injury. https://greenmedinfo.com/article/diosmetin-alleviates-lipopolysaccharide-induced-acute-lung-injury PMID:  Biomol Ther (Seoul). 2018 Mar 1 ;26(2):157-166. PMID: 28365974 Abstract Title:  Diosmetin Alleviates Lipopolysaccharide-Induced Acute Lung Injury through Activating the Nrf2 Pathway and Inhibiting the NLRP3 Inflammasome. Abstract:  Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common clinical syndrome of diffuse lung inflammation with high mortality rates and limited therapeutic methods. Diosmetin, an active component from Chinese herbs, has long been noticed because of its antioxidant and anti-inflammatory activities. The aim of this study was to evaluate the effects of diosmetin on LPS-induced ALI model and unveil the possible mechanisms. Our results revealed that pretreatment with diosmetin effectively alleviated lung histopathological changes, which were further evaluated by lung injury scores. Diosmetin also decreased lung wet/dry ratios, as well as total protein levels, inflammatory cell infiltration and proinflammatory cytokine (eg. TNF-α, IL-1β and IL-6) overproduction in bronchoalveolar lavage fluid (BALF). Additionally, increased MPO, MDA and ROS levels induced by LPS were also markly suppressed by diosmetin. Furthermore, diosmetin significantly increased the expression of Nrf2 along with its target gene HO-1 and blocked the activation of NLRP3 inflammasome in the lung tissues, which might be central to the protective effects of diosmetin. Further supporting these results,experiments also showed that diosmetin activated Nrf2 and HO-1, as well as inhibited the NLRP3 inflammasome in both RAW264.7 and A549 cells. The present study highlights the protective effects of diosmetin on LPS-induced ALI via activation of Nrf2 and inhibition of NLRP3 inflammasome, bringing up the hope of its application as a therapeutic drug towards LPS-induced ALI. <p><a href="https://greenmedinfo.com/article/diosmetin-alleviates-lipopolysaccharide-induced-acute-lung-injury" target="_blank">read more</a></p> https://greenmedinfo.com/article/diosmetin-alleviates-lipopolysaccharide-induced-acute-lung-injury#comments Acute Respiratory Distress Syndrome Diosmetin Lipopolysaccharide-Induced Toxicity Lung Injury: Acute Anti-Inflammatory Agents Antioxidants Heme oxygenase-1 up-regulation Nrf2 activation In Vitro Study Sun, 01 Mar 2020 00:16:54 +0000 greenmedinfo 214855 at https://greenmedinfo.com Electroacupuncture alleviates LPS-induced ARDS through α7 nicotinic acetylcholine receptor-mediated inhibition of ferroptosis. https://greenmedinfo.com/article/electroacupuncture-alleviates-lps-induced-ards-through-7-nicotinic-acetylcholi PMID:  Front Immunol. 2022 ;13:832432. Epub 2022 Feb 10. PMID: 35222419 Abstract Title:  Electroacupuncture Alleviates LPS-Induced ARDS Throughα7 Nicotinic Acetylcholine Receptor-Mediated Inhibition of Ferroptosis. Abstract:  Acute respiratory distress syndrome (ARDS) is an uncontrollable, progressive pulmonary inflammatory disease, and as a common clinical critical disease, there is no effective treatment available. Electroacupuncture (EA) therapy is a type of traditional Chinese medicine physiotherapy that can alleviate the inflammatory response. However, the potential mechanism of EA in the treatment of ARDS is not yet clear. Ferroptosis is a new type of programmed cell death characterized by intracellular iron accumulation and lipid peroxidation. Recently, emerging evidence has shown that ferroptosis is closely related to the occurrence and development of ARDS caused by various pathological factors. Here, we further investigated whether EA-mediated inhibition of ferroptosis in lung tissue could attenuate lipopolysaccharide (LPS)-induced ARDS and explored its underlying mechanisms. In this study, mice were administered LPS intraperitoneally to establish a model of LPS-induced ARDS. We found that EA stimulation could not only reduce the exudation of inflammatory cells and proteins in the alveolar lumen but also significantly alleviate the pathological changes of lung tissue, inhibit the production of proinflammatory cytokines and improve the survival rate of mice. Concurrently, we also found that ferroptosis events occurred in the lung tissue of LPS-induced ARDS mice, manifested by elevated iron levels, ROS production and lipid peroxidation. Intriguingly, our results showed that EA stimulation at the Zusanli (ST36) acupoint activatedα7 nicotinic acetylcholine receptor (α7nAchR) in lung tissue mainly through the sciatic nerve and cervical vagus nerve, thus exerting anti-ferroptosis and pulmonary protective effects. Additionally, these effects were eliminated by methyllycaconitine (MLA), a selective antagonist of α7nAchR.experiments, activation ofα7nAchR protected alveolar epithelial cells from LPS-induced ferroptosis. Furthermore, our experiments showed that the pulmonary protective effects of EA stimulation were effectively reversed by erastin, a ferroptosis activator. Collectively, we demonstrated that EA stimulation could alleviate LPS-induced ARDS by activating α7nAchR to inhibit LPS-induced ferroptosis in alveolar epithelial cells. Targeting and regulating ferroptosis in alveolar epithelial cells may be a potential intervention approach for the treatment of LPS-induced ALI/ARDS in the future. <p><a href="https://greenmedinfo.com/article/electroacupuncture-alleviates-lps-induced-ards-through-7-nicotinic-acetylcholi" target="_blank">read more</a></p> https://greenmedinfo.com/article/electroacupuncture-alleviates-lps-induced-ards-through-7-nicotinic-acetylcholi#comments Acute Respiratory Distress Syndrome Lipopolysaccharide-Induced Toxicity Electroacupuncture In Vitro Study Thu, 12 May 2022 18:14:36 +0000 greenmedinfo 257518 at https://greenmedinfo.com Emodin improves alveolar hypercoagulation and fibrinolytic inhibition and depresses excessive pulmonary inflammation in ARDS. https://greenmedinfo.com/article/emodin-improves-alveolar-hypercoagulation-and-fibrinolytic-inhibition-and-depr PMID:  Int Immunopharmacol. 2020 Nov ;88:107020. Epub 2020 Sep 21. PMID: 33182048 Abstract Title:  Emodin improves alveolar hypercoagulation and inhibits pulmonary inflammation in LPS-provoked ARDS in mice via NF-κB inactivation. Abstract:  BACKGROUND: Alveolar hypercoagulation and pulmonary inflammation are important characteristics and they regulate each other in acute respiratory distress syndrome (ARDS). NF-κB pathway has been confirmed to be involved in regulation of this crosstalk. Emodin, a traditional Chinese herb, shows potent inhibitory effect on NF-κB pathway, but whether it is effective in alveolar hypercoagulation and pulmonary inflammation in ARDS remains to be elucidated.PURPOSE: The aim of this experiment was to evaluate the efficacy of emodin on LPS-provoked alveolar hypercoagulation and excessive pulmonary inflammation in ARDS, and its potential mechanism.METHODS: Mice ARDS was set up through LPS (40 μl, 4 mg/ml) inhalation. Male mice were randomly received with BPS, LPS only, LPS+ emodin (5 mg/kg, 10 mg/kg, 20 mg/kg, respectively) and BAY65-1942, an inhibitor of IKKβ. After 48 h of LPS stimulation, pulmonary pathological injury, expressions of Tissue factor (TF), plasminogen activatorinhibitor (PAI)-1, activated protein C (APC), collagen Ⅰ, collagen III, interleukin (IL) 8, IL-1β and tumor necrosis factor (TNF)-α in lung tissues, as well as concentrations of antithrombin III (AT III), procollagen peptide type III (PIIIP), soluble thrombomodulin (sTM), thrombin antithrombin complex (TAT), myeloperoxidase (MPO) and the percentage of inflammatory cells in bronchoalveolar lavage fluid (BALF) were all determined. NF-κB pathway activation as well as NF-κB DNA binding activity in pulmonary tissue were simultaneously checked.RESULTS: LPS stimulation resulted in obvious lung injury, excessive inflammatory cells infiltration, which all were dose-dependently ameliorated by emodin. Expressions of TF, PAI-1, collagenⅠ and collagen III as well as IL-8, IL-1β and TNF-α in pulmonary tissue were all elevated while APC decreased under LPS provocation, which were all reversed by emodin treatment in dose-dependent manner. LPS promoted the secretions of PIIIP, sTM, TAT and inhibited AT III production in BALF, and resulted in high levels of MPO and the percentage of inflammatory cells in BALF, all of which were significantly and dose-dependently attenuated while AT III production was increased by emodin. Meanwhile, emodin effectively inhibited NF-κB pathway activation and attenuated p65 DNA binding activity induced by LPS inhalation. Emodin and BAY-65-1942 had similar impacts in this experiment.CONCLUSIONS: Emodin improves alveolar hypercoagulation and fibrinolytic inhibition and depresses excessive pulmonary inflammation in ARDS mice in dose-dependent manner via NF-κB inactivation. Our data demonstrate that emodin is expected to be an effective drug in alveolar hypercoagulation and pulmonary inflammation in ARDS. <p><a href="https://greenmedinfo.com/article/emodin-improves-alveolar-hypercoagulation-and-fibrinolytic-inhibition-and-depr" target="_blank">read more</a></p> https://greenmedinfo.com/article/emodin-improves-alveolar-hypercoagulation-and-fibrinolytic-inhibition-and-depr#comments Acute Respiratory Distress Syndrome Emodin Anti-Inflammatory Agents Interleukin-1 beta downregulation Interleukin-8 downregulation NF-kappaB Inhibitor Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Fri, 08 Jan 2021 00:33:41 +0000 greenmedinfo 232497 at https://greenmedinfo.com Exploring the molecular mechanism by which kaempferol attenuates sepsis-related acute respiratory distress syndrome. https://greenmedinfo.com/article/exploring-molecular-mechanism-which-kaempferol-attenuates-sepsis-related-acute PMID:  Curr Comput Aided Drug Des. 2024 Feb 6. Epub 2024 Feb 6. PMID: 38321908 Abstract Title:  Exploring the Molecular Mechanism by which Kaempferol Attenuates Sepsis-related Acute Respiratory Distress Syndrome Based on Network Pharmacology and Experimental Verification. Abstract:  BACKGROUND: Sepsis-related acute respiratory distress syndrome (ARDS) is a fatal disease without effective therapy. Kaempferol is a flavonoid compound extracted from natural plant products; it exerts numerous pharmacological effects. Kaempferol attenuates sepsis-related ARDS; however, the underlying protective mechanism has not been elucidated completely.OBJECTIVE: This study aimed to use network pharmacology and experimental verification to investigate the mechanisms by which kaempferol attenuates sepsis-related ARDS.METHODS: We screened the targets of kaempferol by PharMapper, Swiss Target Prediction, and CTD database. We identified the targets of sepsis-related ARDS by GeneCards, DisGeNet, OMIM, and TTD. The Weishengxin platform was used to map the targets of both kaempferol and sepsis-related ARDS. We created a Venn diagram to identify the intersection targets. We constructed the &quot;component-intersection targets-disease&quot; network diagram using Cytoscape 3.9.1 software. The intersection targets were imported into the STRING database for developing the protein-protein interaction network. Metascape was used for the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. We selected the leading 20 KEGG pathways to establish the KEGG relationship network. Finally, we performed experimental verification to confirm our prediction results.RESULTS: Through database screening, we obtained 502, 360, and 78 kaempferol targets, disease targets of sepsis-related ARDS, and intersection targets, respectively. The core targets consisted of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, albumin (ALB), IL-1β, and AKT serine/ threonine kinase (AKT)1. GO enrichment analysis identified 426 items, which were principally involved in response to lipopolysaccharide, regulation of inflammatory response, inflammatory response, positive regulation of cell migration, positive regulation of cell adhesion, positive regulation of protein phosphorylation, response to hormone, regulation of reactive oxygen species (ROS) metabolic process, negative regulation of apoptotic signaling pathway, and response to decreased oxygen levels. KEGG enrichment analysis identified 151 pathways. After eliminating the disease and generalized pathways, we obtained the hypoxia-inducible factor 1 (HIF-1), nuclear factorκB (NF-κB), and phosphoinositide 3-kinase (PI3K)-Akt signaling pathways. Our experimental verification confirmed that kaempferol blocked the HIF-1, NF-κB, and PI3K-Akt signaling pathways, diminished TNF-α, IL-1β, and IL-6 expressions, suppressed ROS production, and inhibited apoptosis in lipopolysaccharide (LPS)-induced murine alveolar macrophage (MH-S) cells.CONCLUSION: Kaempferol can reduce inflammatory response, ROS production, and cell apoptosis by acting on the HIF-1, NF-κB, and PI3K-Akt signaling pathways, thereby alleviating sepsis- related ARDS. <p><a href="https://greenmedinfo.com/article/exploring-molecular-mechanism-which-kaempferol-attenuates-sepsis-related-acute" target="_blank">read more</a></p> https://greenmedinfo.com/article/exploring-molecular-mechanism-which-kaempferol-attenuates-sepsis-related-acute#comments Acute Respiratory Distress Syndrome Kaempferol Sepsis Anti-Inflammatory Agents Hypoxia-inducible factor-1 (HIF-1) inhibitor Interleukin-1 beta downregulation Interleukin-6 Downregulation NF-kappaB Inhibitor Tumor Necrosis Factor (TNF) Alpha Inhibitor In Vitro Study Sat, 10 Feb 2024 20:53:04 +0000 greenmedinfo 288164 at https://greenmedinfo.com Fatal lupus-like syndrome and ARDS induced by fluvastatin has been reported. https://greenmedinfo.com/article/fatal-lupus-syndrome-and-ards-induced-fluvastatin-has-been-reported PMID:  Lancet. 1998 Jul 11 ;352(9122):114. PMID: 9672281 Abstract Title:  Fatal lupus-like syndrome and ARDS induced by fluvastatin. Abstract:  No abstract is available. https://greenmedinfo.com/article/fatal-lupus-syndrome-and-ards-induced-fluvastatin-has-been-reported#comments Acute Respiratory Distress Syndrome Lupus-Like Syndrome Anticholesteremic Agents Fluvastatin Human: Case Report Mon, 24 Oct 2011 18:38:49 +0000 greenmedinfo 69216 at https://greenmedinfo.com Florida red tide results in a 54% increase in the rate of respiratory diagnoses admissions than during the red tide period. https://greenmedinfo.com/article/florida-red-tide-results-54-increase-rate-respiratory-diagnoses-admissions-dur PMID:  Harmful Algae. 2006 Oct 1 ;5(5):526-533. PMID: 20357898 Abstract Title:  Environmental exposures to Florida red tides: Effects on emergency room respiratory diagnoses admissions. Abstract:  Human exposure to Florida red tides formed by Karenia brevis, occurs from eating contaminated shellfish and inhaling aerosolized brevetoxins. Recent studies have documented acute symptom changes and pulmonary function responses after inhalation of the toxic aerosols, particularly among asthmatics. These findings suggest that there are increases in medical care facility visits for respiratory complaints and for exacerbations of underlying respiratory diseases associated with the occurrence of Florida red tides.This study examined whether the presence of a Florida red tide affected the rates of admission with a respiratory diagnosis to a hospital emergency room in Sarasota, FL. The rate of respiratory diagnoses admissions were compared for a 3-month time period when there was an onshore red tide in 2001 (red tide period) and during the same 3-month period in 2002 when no red tide bloom occurred (non-red tide period). There was no significant increase in the total number of respiratory admissions between the two time periods. However, there was a 19% increase in the rate of pneumonia cases diagnosed during the red tide period compared with the non-red tide period. We categorized home residence zip codes as coastal (within 1.6 km from the shore) or inland (&gt;1.6 km from shore). Compared with the non-red tide period, the coastal residents had a significantly higher (54%) rate of respiratory diagnoses admissions than during the red tide period. We then divided the diagnoses into subcategories (i.e. pneumonia, bronchitis, asthma, and upper airway disease). When compared with the non-red tide period, the coastal zip codes had increases in the rates of admission of each of the subcategories during the red tide period (i.e. 31, 56, 44, and 64%, respectively). This increase was not observed seen in the inland zip codes.These results suggest that the healthcare community has a significant burden from patients, particularly those who live along the coast, needing emergency medical care for both acute and potentially chronic respiratory illnesses during red tide blooms. https://greenmedinfo.com/article/florida-red-tide-results-54-increase-rate-respiratory-diagnoses-admissions-dur#comments Acute Respiratory Distress Syndrome Asthma Red Tide Associated Toxicity Respiratory Diseases Red tide Human Study Tue, 06 Dec 2011 18:28:04 +0000 greenmedinfo 70151 at https://greenmedinfo.com Hesperidin a positive immunomodulatory effect in a clinically relevant model of Acute Respiratory Distress Syndrome. https://greenmedinfo.com/article/hesperidin-positive-immunomodulatory-effect-clinically-relevant-model-acute-re PMID:  Life Sci. 2007 Apr 24;80(20):1821-31. Epub 2007 Feb 3. PMID: 17400256 Abstract Title:  The immunomodulation of endotoxin-induced acute lung injury by hesperidin in vivo and in vitro. Abstract:  To investigate the modulation of lung local immune responses of hesperidin (HES) on the acute lung inflammation induced by LPS in vivo. Mice were challenged with intratracheal lipopolysaccharide (100 microg) 30 min before with treatment hesperidin (200 mg/kg oral administration) or vehicle. After 4 and 24 h, bronchoalveolar lavage fluid was obtained to measure proinflammatory (TNF-alpha, IL-1 beta, IL-6), anti-inflammatory (IL-10, IL-4, IL-12) cytokines, chemokines (KC, MCP-1 and MIP-2), total cell counts, nitric oxide production, and proteins. Lung histology was performed in inflated-fixed lungs. Hesperidin downregulate the LPS-induced expression of TNF-alpha, IL-1 beta, IL-6, KC, MIP-2, MCP-1, and IL-12. It also enhanced the production of IL-4, IL-10. Total leukocyte counts; nitric oxide production, iNOS expression, and proteins were significantly decreased by hesperidin. In vitro, HES suppressed the expression of IL-8 on A549 cells and THP-1 cells, the expression of TNF-alpha, IL-1 beta, and IL-6 on THP-1 cells, the expression of ICAM-1 and VCAM-1 on A549 cells which effect cell adhesion function. The suppression of those molecules is controlled by NF-kappaB and AP-1, which are activated by I kappa B and MAPK pathways. HES inhibits those pathways, thereby suppressing the expression of IL-8, TNFalpha, IL-1 beta, IL-6, IL-12, ICAM-1 and VCAM-1. This study indicates that HES had a markedly immunomodulatory effect in a clinically relevant model of ARDS. Nevertheless, further investigations are required to determine the potential clinical usefulness of HES in the adjunctive therapy of ARDS.   https://greenmedinfo.com/article/hesperidin-positive-immunomodulatory-effect-clinically-relevant-model-acute-re#comments Acute Respiratory Distress Syndrome Hesperidin Interleukin-6 Downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor Animal Study Mon, 20 Apr 2009 06:14:13 +0000 greenmedinfo 42648 at https://greenmedinfo.com