Encephalopathy https://greenmedinfo.com/taxonomy/term/74438/all en Report of a 6-month-old Asian infant with early infantile epileptic encephalopathy whose seizures were eliminated by cannabidiol. https://greenmedinfo.com/article/report-6-month-old-asian-infant-early-infantile-epileptic-encephalopathy-whose PMID:  Epilepsy Behav Rep. 2020 ;14:100373. Epub 2020 Jun 8. PMID: 32695984 Abstract Title:  Report of a 6-month-old Asian infant with early infantile epileptic encephalopathy whose seizures were eliminated by cannabidiol. Abstract:  We observed that cannabidiol supplements were highly effective in treating an infant boy with drug-resistant early infantile epileptic encephalopathy, eliminating his intractable tonic seizures. The infant began suffering clusters of brief tonic seizures from birth at 39 weeks gestation. EEG showed burst-suppression and seizures could not be controlled by trials of phenobarbital, zonisamide, vitamin B6, clobazam, levetiracetam, topiramate, phenytoin, valproate, high-dose phenobarbital, and ACTH therapy. The boy was discharged from hospital at 130 days of age still averaging tonic seizures 20-30 times per day. We started him on a cannabidiol supplement on day 207, increasing the dosage to 18 mg/kg/d on day 219. His seizures reduced in frequency and completely disappeared by day 234. These effects were maintained, with improved EEG background, even afterhis other medications were discontinued. Cannabidiol&#039;s effectiveness in treating drug-resistant epilepsy has been confirmed in large-scale clinical trials in Europe and the United States; however, no such trials have been run in Asia. In addition, no reports to date have documented its efficacy in an infant as young as six months of age. This important case suggests that high-dose artisanal cannabidiol may effectively treat drug-resistant epilepsy in patients without access to pharmaceutical-grade CBD. <p><a href="https://greenmedinfo.com/article/report-6-month-old-asian-infant-early-infantile-epileptic-encephalopathy-whose" target="_blank">read more</a></p> https://greenmedinfo.com/article/report-6-month-old-asian-infant-early-infantile-epileptic-encephalopathy-whose#comments Cannabidiol Encephalopathy Epilepsy Anticonvulsants Significant Treatment Outcome Human: Case Report Mon, 03 Aug 2020 19:51:01 +0000 greenmedinfo 224658 at https://greenmedinfo.com Aluminum has been recurrently shown to cause encephalopathy and is connected to Alzheimer's disease. https://greenmedinfo.com/article/aluminum-has-been-recurrently-shown-cause-encephalopathy-and-connected-alzheim PMID:  Adv Neurobiol. 2017 ;18:183-197. PMID: 28889268 Abstract Title:  Aluminum and Alzheimer&#039;s Disease. Abstract:  Aluminum (Al) is one of the most extended metals in the Earth&#039;s crust. Its abundance, together with the widespread use by humans, makes Al-related toxicity particularly relevant for human health.Despite some factors influence individual bioavailability to this metal after oral, dermal, or inhalation exposures, humans are considered to be protected against Al toxicity because of its low absorption and efficient renal excretion. However, several factors can modify Al absorption and distribution through the body, which may in turn progressively contribute to the development of silent chronic exposures that may lately trigger undesirable consequences to health. For instance, Al has been recurrently shown to cause encephalopathy, anemia, and bone disease in dialyzed patients. On the other hand, it remains controversial whether low doses of this metal may contribute to developing Alzheimer&#039;s disease (AD), probably because of the multifactorial and highly variable presentation of the disease.This chapter primarily focuses on two key aspects related to Al neurotoxicity and AD, which are metabolic impairment and iron (Fe) alterations. We discuss sex and genetic differences as a plausible source of bias to assess risk assessment in human populations. <p><a href="https://greenmedinfo.com/article/aluminum-has-been-recurrently-shown-cause-encephalopathy-and-connected-alzheim" target="_blank">read more</a></p> https://greenmedinfo.com/article/aluminum-has-been-recurrently-shown-cause-encephalopathy-and-connected-alzheim#comments Anemia Encephalopathy Neurodegenerative Diseases Oxidative Stress Aluminum Neurotoxic Vaccination: All Review Thu, 21 Nov 2019 22:26:06 +0000 greenmedinfo 202364 at https://greenmedinfo.com Berberine alleviates the damage, oxidative stress and mitochondrial dysfunction of PC12 cells induced by high glucose. https://greenmedinfo.com/article/berberine-alleviates-damage-oxidative-stress-and-mitochondrial-dysfunction-pc1 PMID:  Mol Biotechnol. 2023 Feb 3. Epub 2023 Feb 3. PMID: 36737555 Abstract Title:  Berberine Alleviates the Damage, Oxidative Stress and Mitochondrial Dysfunction of PC12 Cells Induced by High Glucose by Activating the KEAP1/Nrf2/ARE Pathway. Abstract:  Diabetic encephalopathy (DE) is one of the major chronic complications of diabetes mellitus. This study aims to investigate the inhibitory effect of berberine (BBR) on the damage of PC12 cells induced by high glucose (HG). Differentiated PC12 cells were treated with different concentrations of glucose/BBR. The cell morphology, cell viability, lactate dehydrogenase (LDH) activity, apoptosis, oxidative stress (OS), mitochondrial structure, mitochondrial membrane potential (MMP), mitochondrial complex I-V activity, and adenosine triphosphate (ATP) levels were evaluated. The mRNA and protein levels of the Keap1/Nrf2/ARE pathway-related genes were assessed by RT-qPCR and Western blot. High-dose BBR and HG jointly treated-PC12 cells were treated with Nrf2-specific inhibitor ML385 to further verify whether Nrf2 was the target of BBR. The results showed that BBR inhibited cell damage, OS, and mitochondrial dysfunction induced by HG. The inhibitory effect of high BBR was more significant. The Keap1/Nrf2/ARE pathway was inhibited in PC12 cells induced by HG. BBR could activate the Keap1/Nrf2/ARE pathway, thus up-regulating the expression levels of antioxidant enzymes. ML385 antagonized the ameliorating effect of BBR on OS and mitochondrial dysfunction. The conclusion is that BBR can activate the Keap1/Nrf2/ARE pathway, upregulate the expression patterns of antioxidant enzymes, and reduce cell damage, OS, and mitochondrial dysfunction of PC12 cells induced by HG. <p><a href="https://greenmedinfo.com/article/berberine-alleviates-damage-oxidative-stress-and-mitochondrial-dysfunction-pc1" target="_blank">read more</a></p> https://greenmedinfo.com/article/berberine-alleviates-damage-oxidative-stress-and-mitochondrial-dysfunction-pc1#comments Berberine Diabetic Complications Encephalopathy Antioxidants Nrf2 activation In Vitro Study Sun, 12 Feb 2023 23:47:50 +0000 greenmedinfo 271005 at https://greenmedinfo.com Carnosine improves cognitive impairment through promoting SIRT6 expression and inhibiting ER stress in a diabetic encephalopathy model. https://greenmedinfo.com/article/carnosine-improves-cognitive-impairment-through-promoting-sirt6-expression-and PMID:  Rejuvenation Res. 2022 Mar 18. Epub 2022 Mar 18. PMID: 35302398 Abstract Title:  Carnosine improves cognitive impairment through promoting SIRT6 expression and inhibiting ER stress in a diabetic encephalopathy model. Abstract:  Diabetic encephalopathy is one of complications of diabetes mellitus. Carnosine is a dipeptide composed ofβ-alanine and L-histidine. Study has shown that carnosine could ameliorate cognitive impairment in animal model with diabetes mellitus. However, the mechanism remains unclear. An animal model of type 2 diabetes (db/db mice) was used in this study. The animals were treated with 0.9 % saline or carnosine (100 mg/kg) for 8 weeks. Morris water maze was tested after drug administration. Oxidative stress-related factors malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), and pro-inflammatory factors inducible nitric oxide synthase (iNOS) were measured. Synapse-related protein postsynapticdensity 95 (PSD95) and brain-derived neurotrophic factor (BDNF) were detected by western blot. Besides, the expressions of sirtuin 6 (SIRT6), binding immunoglobulin protein (BIP), protein kinase R-like endoplasmic reticulum kinase (PERK), phospho-protein kinaseR-like endoplasmic reticulum kinase (P-PERK), inositol-requiring enzyme-1α (IRE1α), phospho-inositol-requiring enzyme-1α (P-IRE1α), activating transcription factor 6 (ATF6), C/EBP-homologous protein (CHOP) in the hippocampus of the brain were detected. The results showed that treatment with carnosine ameliorated cognitive impairment in db/db mice. Carnosine reduced neuronal oxidative stress damage and iNOS expression in db/db mice. Meanwhile, carnosine relieved neurodegeneration in the hippocampus of db/db mice. Furthermore, carnosine promoted the expression of SIRT6 and reduced the expressions of endoplasmic reticulum (ER) related factors (BIP, P-PERK, P-IRE1α, ATF6, CHOP). In conclusion, these data suggested that the protective effect of carnosine against diabetic encephalopathy might be related to SIRT6/ER stress pathway. <p><a href="https://greenmedinfo.com/article/carnosine-improves-cognitive-impairment-through-promoting-sirt6-expression-and" target="_blank">read more</a></p> https://greenmedinfo.com/article/carnosine-improves-cognitive-impairment-through-promoting-sirt6-expression-and#comments Carnosine Diabetes: Cognitive Dysfunction Encephalopathy Neuroprotective Agents Animal Study Sat, 26 Mar 2022 02:42:31 +0000 greenmedinfo 255287 at https://greenmedinfo.com Chlorogenic acid may improve memory function and decrease inflamation of frontal lobe. https://greenmedinfo.com/article/chlorogenic-acid-may-improve-memory-function-and-decrease-inflamation-frontal- PMID:  Med J Malaysia. 2023 Jul ;78(4):476-483. PMID: 37518915 Abstract Title:  Chlorogenic acid may improve memory function and decrease inflamation of frontal lobe in diabetic rat. Abstract:  INTRODUCTION: Diabetes Mellitus (DM) is a chronic disease with many complications, one of which is diabetic encephalopathy which is characterised by memory dysfunction. Hyperglycaemia that occurs in DM will activate inflammatory pathways in neurons, including NF-κB pathway. Activation of this pathway produce proinflammatory agents such as MCP-1 and IL-6, which activate glial cells. Activation of glial cells is characterised by Glial Fibrillary Acid Protein (GFAP). Chlorogenic acid (CGA) has been reported to have anti-inflammatory effects and can improve memory function. This research aimed to determine the effect of CGA as anti-inflammation, its effect on memory function, mRNA expression of NF-κB, MCP-1, IL- 6, and GFAP of frontal lobe.MATERIALS AND METHODS: A total of 24 male rats were randomly divided into six groups: control, DM 1.5 month (DM1.5), DM 2 months (DM2) and the group with three different doses of CGA 12.5 (CGA1), 25 (CGA2), and 50 (CGA3) mg/KgBW. Frontal lobe tissue is taken for analysis of mRNA expression for NF-κB, MCP-1, IL-6, and GFAP using Reverse Transcriptase PCR (RT-PCR). Samples were also taken for histopathology preparation and stained by immunohistochemistry method using anti-GFAP antibodies to observe glial cell activation in frontal lobe tissue.RESULTS: The group that was given CGA at all doses have statistically significant better memory function, i.e. DM2 versus CGA1 (p = 0.036), CGA2 (p = 0.040), and CGA3 (p = 0.021). The result of mRNA expression in NF-κB was lower in the group given CGA, i.e. DM2 compared to CGA2 (p = 0.007). mRNA expression of MCP-1 was significantly lower in all CGA treatment groups compared to the non-CGA group (p = 0.000). IL-6 mRNA expression was lower than the group not given CGA, DM compared to CGA2 (p = 0.028). GFAP mRNA expression was lower than the group given CGA in DM, DM2 group compared to CGA1 (p = 0.04) and CGA3 (p = 0.004).CONCLUSION: Administration of CGA can improve memory function at all doses given, and can reduce brain inflammatory activity, especially in the CGA2 group. <p><a href="https://greenmedinfo.com/article/chlorogenic-acid-may-improve-memory-function-and-decrease-inflamation-frontal-" target="_blank">read more</a></p> https://greenmedinfo.com/article/chlorogenic-acid-may-improve-memory-function-and-decrease-inflamation-frontal-#comments Brain Inflammation Chlorogenic Acid Encephalopathy Anti-Inflammatory Agents Interleukin-6 Downregulation Neuroprotective Agents NF-kappaB Inhibitor Animal Study Wed, 18 Oct 2023 00:10:04 +0000 greenmedinfo 282388 at https://greenmedinfo.com Clone of Measles and Measles Vaccines: 14 Things To Consider https://greenmedinfo.com/blog/clone-measles-and-measles-vaccines-14-things-consider <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2014<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p></p> <p class="rteleft"><strong><em>There are facts regarding the history of measles that almost never reach the light of day. Here are 14 things you may not have been told by public health officials, your doctor, or the media.</em></strong></p> <p>Article Originally Published <strong>Here</strong></p><p><a href="https://greenmedinfo.com/blog/clone-measles-and-measles-vaccines-14-things-consider" target="_blank">read more</a></p> https://greenmedinfo.com/blog/clone-measles-and-measles-vaccines-14-things-consider#comments Asthma Cinnamon Encephalopathy Influenza Magnesium Manganese Measles Omega-3 Fatty Acids Pneumonia Potassium Rubella Varicella Vitamin A Vitamin C Zinc Breastfeeding Vaccination: All Vaccination: Measles Vaccination: Mumps-Measles-Rubella (MMR) Vaccination: Smallpox Asthma breastfeeding CDC cinnamon Encephalopathy influenza Magnesium manganese Measles MMR Vaccine omega-3 fatty acids Pneumonia potassium Rubella Smallpox Vaccine Vaccine Varicella Vitamin A Vitamin C zinc Tue, 14 Oct 2014 12:49:25 +0000 Sayer Ji 114975 at https://greenmedinfo.com Diabetic encephalopathy: beneficial effects of supplementation with fatty acids ω3 and nordihydroguaiaretic acid. https://greenmedinfo.com/article/diabetic-encephalopathy-beneficial-effects-supplementation-fatty-acids-3-and-n PMID:  Lipids Health Dis. 2019 Feb 8 ;18(1):43. Epub 2019 Feb 8. PMID: 30736810 Abstract Title:  Diabetic encephalopathy: beneficial effects of supplementation with fatty acidsω3 and nordihydroguaiaretic acid in a spontaneous diabetes rat model. Abstract:  BACKGROUND: Diabetic encephalopathy is a chronic complications of diabetes mellitus that affects the central nervous system. We evaluated the effect ofω3 and ω6 polyunsaturated fatty acids (PUFAs) supplementation plus the antioxidant agent nordihydroguaiaretic acid (NDGA) on the etiopathology of diabetic encephalopathy in eSS rats, a spontaneous model of type 2 diabetes.METHODS: One hundred twenty spontaneous diabetic eSS male rats and 38 non-diabetic Wistar, used as healthy control, received monthly by intraperitoneal route,ω3 or ω6 PUFA (6.25 mg/kg) alone or plus NDGA (1.19 mg/kg) for 12 months. Diabetic rats had a worse performance in behavioural Hole-Board test. Histopathological analysis confirmed lesions in diabetic rats brain tissues. We also detected low expression of synaptophysin, a protein linked torelease of neurotransmitters, by immunohistochemically techniques in eSS rats brain. Biochemical and histopathological studies of brain were performed at 12th month. Biochemical analysis showed altered parameters related to metabolism. High levels of markers of oxidative stress and inflammation were detected in plasma and brain tissues. Data were analysed by ANOVA test and paired t test was used by comparison of measurements of the same parameter at different times.RESULTS: The data obtained in this work showed that behavioural, biochemical and morphological alterations observed in eSS rats are compatible with previously reported indices in diabetic encephalopathy and are associated with increased glucolipotoxicity, chronic low-grade inflammation and oxidative stress burden. Experimental treatments assayed modulated the values of studied parameters.CONCLUSIONS: The treatments tested withω3 or ω3 plus NDGA showed improvement in the values of the studied parameters in eSS diabetic rats. These observations may form the basis to help in prevent and manage the diabetic encephalopathy. <p><a href="https://greenmedinfo.com/article/diabetic-encephalopathy-beneficial-effects-supplementation-fatty-acids-3-and-n" target="_blank">read more</a></p> https://greenmedinfo.com/article/diabetic-encephalopathy-beneficial-effects-supplementation-fatty-acids-3-and-n#comments Diabetes: Oxidative Stress Encephalopathy Nordihydroguaiaretic acid (NDGA) Omega-3 Fatty Acids Anti-Inflammatory Agents Antioxidants Animal Study Sun, 16 Feb 2020 22:12:48 +0000 greenmedinfo 212156 at https://greenmedinfo.com Dietary approach and gut microbiota modulation for chronic hepatic encephalopathy in cirrhosis. https://greenmedinfo.com/article/dietary-approach-and-gut-microbiota-modulation-chronic-hepatic-encephalopathy- PMID:  World J Hepatol. 2019 Jun 27 ;11(6):489-512. PMID: 31293718 Abstract Title:  Dietary approach and gut microbiota modulation for chronic hepatic encephalopathy in cirrhosis. Abstract:  Hepatic encephalopathy (HE) is a common and serious neuropsychiatric complication of cirrhosis, acute liver failure, and porto-systemic shunting. HE largely contributes to the morbidity of patients with liver disease, severely affecting the quality of life of both patients and their relatives and being associated with poor prognosis. Its presentation is largely variable, manifesting with a broad spectrum of cognitive abnormalities ranging from subtle cognitive impairment to coma. The pathogenesis of HE is complex and has historically been linked with hyperammonemia. However, in the last years, it has become evident that the interplay of multiple actors, such as intestinal dysbiosis, gut hyperpermeability, and neuroinflammation, is of crucial importance in its genesis. Therefore, HE can be considered a result of a dysregulated gut-liver-brain axis function, where cognitive impairment can be reversed or prevented by the beneficial effects induced by&quot;gut-centric&quot;therapies, such as non-absorbable disaccharides, non-absorbable antibiotics, probiotics, prebiotics, and fecal microbiota transplantation. In this context dietary modifications, by modulating the intestinal milieu, can also provide significant benefit to cirrhotic patients with HE. This review will provide a comprehensive insight into the mechanisms responsible for gut-liver-brain axis dysregulation leading to HE in cirrhosis. Furthermore, it will explore the currently available therapies and the most promising future treatments for the management of patients with HE, with a special focus on the dietary approach. <p><a href="https://greenmedinfo.com/article/dietary-approach-and-gut-microbiota-modulation-chronic-hepatic-encephalopathy-" target="_blank">read more</a></p> https://greenmedinfo.com/article/dietary-approach-and-gut-microbiota-modulation-chronic-hepatic-encephalopathy-#comments Cirrhosis Encephalopathy Prebiotics Probiotics Gastrointestinal Agents Microbiota Transfer Therapy Gut-liver axis Microbiota Review Tue, 06 Aug 2019 18:52:06 +0000 greenmedinfo 192974 at https://greenmedinfo.com Effectiveness of cannabidiol in a prospective cohort of children with drug-resistant epileptic encephalopathy. https://greenmedinfo.com/article/effectiveness-cannabidiol-prospective-cohort-children-drug-resistant-epileptic PMID:  Seizure. 2020 Jun 6 ;80:75-80. Epub 2020 Jun 6. PMID: 32544657 Abstract Title:  Effectiveness of cannabidiol in a prospective cohort of children with drug-resistant epileptic encephalopathy in Argentina. Abstract:  OBJECTIVE: We report our preliminary findings regarding effectiveness, safety, and tolerability of cannabidiol (CBD) added to antiepileptic therapy in a cohort of children with drug-resistant epileptic encephalopathies (EEs) with a mean follow-up of 8.5 months (range, 3-12 months).METHODS: A prospective cohort study was designed with the aim of assessing the effectiveness, safety, and tolerability of the addition of CBD to standard antiseizure medications (ASMs) in children with drug-resistant EE enrolled at a single center (Neurology Department, Hospital de Pediatría&quot;Juan P. Garrahan&quot;, Buenos Aires, Argentina).RESULTS: Fifty patients were enrolled between October 2018 and October 2019, 49 of whom had a follow-up of at least 3 months at the time this interim analysis was performed. Mean age at enrollment was 10.5 years (range 2-16). Median age at first seizure was 7 months. Up to the last visit of each patient (follow-up 3-12 months) 39/49 children (80 %) had responded to treatment with a decrease in seizure frequency. Overall, 77.6 % of the patients had a seizure reduction of at least 25 %, 73.5 % had a≥ 50 % reduction, and 49 % had a ≥ 75 % reduction. Mean monthly seizure frequency was reduced from 959 to 381 (median decrease from 299 to 102, range, 38-1900; median decrease 66 %, p<p><a href="https://greenmedinfo.com/article/effectiveness-cannabidiol-prospective-cohort-children-drug-resistant-epileptic" target="_blank">read more</a></p> https://greenmedinfo.com/article/effectiveness-cannabidiol-prospective-cohort-children-drug-resistant-epileptic#comments Cannabidiol Encephalopathy Anticonvulsants Human Study Sat, 04 Jul 2020 20:29:26 +0000 greenmedinfo 223133 at https://greenmedinfo.com Electroacupuncture may protect against sepsis-associated encephalopathy-induced cognitive dysfunction. https://greenmedinfo.com/article/electroacupuncture-may-protect-against-sepsis-associated-encephalopathy-induce PMID:  J Surg Res. 2020 Jul 23 ;256:258-266. Epub 2020 Jul 23. PMID: 32712439 Abstract Title:  Electroacupuncture Improves Cognition in Rats With Sepsis-Associated Encephalopathy. Abstract:  BACKGROUND: Sepsis-associated encephalopathy (SAE) is a common complication of sepsis. Although sepsis is effectively managed with the administration of antibiotics and source control, which may include surgical intervention, SAE usually leads to prolonged cognitive dysfunction affecting the quality of life of the patients. In this study, we investigated the possible effect of electroacupuncture (EA) on cognition in a model of SAE induced by cecal ligation and puncture (CLP).MATERIALS AND METHODS: The rats were randomly divided into four groups: the control group, the CLP group, the CLP with EA treatment group (CLP + EA), and the CLP with sham EA treatment group (CLP + sham EA). EA at DU20, LI11, and ST36 or sham EA was performed 30 min daily for 10 consecutive days starting from 2 days before CLP. Then cognitive function was examined by the Morris water maze test. On day 14 after CLP surgery, the synaptic injury, neuron loss, and oxidative stress were studied.RESULTS: Rats with EA treatment showed improved survival rate, spatial learning, and memory abilities. The dendritic spine density, the synaptic proteins, and the hippocampal neuron number were also increased after EA treatment. Furthermore, EA suppressed oxidative stress through regulating the level of malondialdehyde and superoxide dismutase and enhanced the expression of antioxidant nuclear factor erythroid-2-related factor-2 and hemeoxygenase-1. But sham EA did not have the same effect.CONCLUSIONS: EA may protect against SAE-induced cognitive dysfunction by inhibiting synaptic injury, neuronal loss, and oxidative stress, and the nuclear factor erythroid-2-related factor-2/hemeoxygenase-1 signaling pathway may be involved in this effect. <p><a href="https://greenmedinfo.com/article/electroacupuncture-may-protect-against-sepsis-associated-encephalopathy-induce" target="_blank">read more</a></p> https://greenmedinfo.com/article/electroacupuncture-may-protect-against-sepsis-associated-encephalopathy-induce#comments Encephalopathy Sepsis Antioxidants Electroacupuncture Neuroprotective Agents Nrf2 activation Animal Study Tue, 28 Jul 2020 22:01:11 +0000 greenmedinfo 224354 at https://greenmedinfo.com Epicatechin reduces neuroinflammation, protects mitochondria function, and prevents cognitive impairment in sepsis-associated encephalopathy. https://greenmedinfo.com/article/epicatechin-reduces-neuroinflammation-protects-mitochondria-function-and-preve PMID:  Oxid Med Cell Longev. 2022 ;2022:2657713. Epub 2022 May 24. PMID: 35656027 Abstract Title:  (-)-Epicatechin Reduces Neuroinflammation, Protects Mitochondria Function, and Prevents Cognitive Impairment in Sepsis-Associated Encephalopathy. Abstract:  Sepsis-associated encephalopathy is a common neurological complication of sepsis. Despite advances in pathological and diagnostic investigations, its treatment remains a major challenge. In sepsis-associated encephalopathy, neuroinflammatory overactivation and mitochondrial damage are thought to contribute to cognitive and behavioral impairments. In this study, we found that administration of (-)-Epicatechin, a dietary flavonoid of the flavan-3-ol subgroup, improves memory deficits and behavior performance by ameliorating neuroinflammation, regulating mitochondria function, enhancing synaptic plasticity, and reducing neuronal loss in a mouse model of lipopolysaccharide-induced sepsis. We further show that the AMPK signaling pathway might be among the mechanisms involved in the beneficial memory effects. Our data demonstrated the potential of (-)-Epicatechin as a new drug candidate for the treatment of sepsis-associated cognitive impairment by targeting AMPK. <p><a href="https://greenmedinfo.com/article/epicatechin-reduces-neuroinflammation-protects-mitochondria-function-and-preve" target="_blank">read more</a></p> https://greenmedinfo.com/article/epicatechin-reduces-neuroinflammation-protects-mitochondria-function-and-preve#comments Catechin Cognitive Decline/Dysfunction Encephalopathy Sepsis Neuroprotective Agents Animal Study Thu, 09 Jun 2022 22:25:29 +0000 greenmedinfo 258864 at https://greenmedinfo.com Farrerol alleviates hypoxic-ischemic encephalopathy by inhibiting ferroptosis. https://greenmedinfo.com/article/farrerol-alleviates-hypoxic-ischemic-encephalopathy-inhibiting-ferroptosis PMID:  Physiol Res. 2023 Aug 31 ;72(4):511-520. PMID: 37795893 Abstract Title:  Farrerol Alleviates Hypoxic-Ischemic Encephalopathy by Inhibiting Ferroptosis in Neonatal Rats via the Nrf2 Pathway. Abstract:  Farrerol (FA) is a traditional Chinese herbal medicine known for its anti-inflammatory and anti-oxidative properties in various diseases. Ferroptosis is an iron-dependent oxidative stress-induced cell death. It is characterized by lipid peroxidation and glutathione depletion and is involved in neuronal injury. However, the role of FA in inhibiting ferroptosis in hypoxic-ischemic encephalopathy (HIE) and its underlying mechanisms are not yet completely elucidated. This study aimed to investigate whether FA could mediate ferroptosis and explore its function and molecular mechanism in HIE. A neonatal rat model of HIE was used, and rats were treated with FA, ML385 (a specific inhibitor of nuclear factor erythroid 2-related factor 2 [Nrf2]), or a combination of both. Neurological deficits, infarction volume, brain water content, pathological changes, and iron ion accumulation in the brain tissues were measured using the Zea-Longa scoring system and triphenyl tetrazolium chloride (TTC), hematoxylin-eosin (HE), and Perls&#039; staining. The expression levels of GSH-Px, MDA, SOD, and ROS in brain tissues were also evaluated. Western blot analysis was performed to analyze the expression of the Nrf2 pathway and ferroptosis-related proteins. The results showed that FA administration significantly reduced neuronal damage, infarct volume, cerebral edema, and iron ion accumulation and inhibited MDA and ROS levels while promoting GSH-Px and SOD levels. FA also increased the expression levels of glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), Nrf2, and HO-1. Moreover, the combination of ML385 and FA in HIE abolished the FA protective effects. Therefore, the study concludes that FA exerts a neuroprotective effect after HIE by inhibiting oxidative stress and ferroptosis via the Nrf2 signaling pathway. <p><a href="https://greenmedinfo.com/article/farrerol-alleviates-hypoxic-ischemic-encephalopathy-inhibiting-ferroptosis" target="_blank">read more</a></p> https://greenmedinfo.com/article/farrerol-alleviates-hypoxic-ischemic-encephalopathy-inhibiting-ferroptosis#comments Encephalopathy Flavonoids Antioxidants Heme oxygenase-1 up-regulation Nrf2 activation Superoxide Dismutase Up-regulation Animal Study Mon, 20 Nov 2023 21:01:15 +0000 greenmedinfo 283689 at https://greenmedinfo.com Ginsenoside Rg1 protects against sepsis-associated encephalopathy. https://greenmedinfo.com/article/ginsenoside-rg1-protects-against-sepsis-associated-encephalopathy PMID:  J Surg Res. 2017 01 ;207:181-189. Epub 2016 Aug 31. PMID: 27979475 Abstract Title:  Ginsenoside Rg1 protects against sepsis-associated encephalopathy through beclin 1-independent autophagy in mice. Abstract:  BACKGROUND: Sepsis-associated encephalopathy (SAE), a commonly complicated syndrome, is associated with increased mortality in patients with sepsis. Currently, no specific diagnostic test or effective intervention exists to improve long-term consequences on cerebral function. Ginsenoside Rg1 (Rg1), a major component in ginseng, was reported to have pleiotropic properties including anti-inflammation and neuroprotection. The aim of our study was to investigate the protective effect of Rg1 on SAE and the potential mechanism.MATERIALS AND METHODS: SAE model was prepared by inducing cecal ligation and puncture (CLP) in mice. Rg1 was injected 1 h before the CLP operation. Survival rate within 7 d after operation was analyzed. Surviving mice were subjected to Morris water maze tests and the brains were collected for histopathologic evaluation and immunohistochemistry. The hippocampus was obtained for Western blot, real time polymerase chain reaction, and enzyme-linked immunosorbent assay analysis.RESULTS: Rg1 improved the postoperative survival rate and protected against sepsis-associated learning and memory impairments (Morris water maze). Besides, Rg1 was able to attenuate brain histopathologic changes (hematoxylin and eosin staining), suppress Iba1 activation, decrease the expressions of inflammatory cytokines (tumor necrosis factorα, interleukin 1β, and interleukin 6), and reduce neuronal apoptosis (cleaved caspase 3 activation) in hippocampus. Furthermore, the mechanism study showed that Rg1 suppressed the expressions of light chain 3-II and p62 in hippocampus but not beclin 1.CONCLUSIONS: These findings suggested that Rg1 improved the survival rate and ameliorated cognitive impairments partially through regulating cerebral inflammation and apoptosis. In addition, the action mechanism might be noncanonical beclin 1-independent autophagy pathway. Rg1 may be a promising treatment strategy for SAE. <p><a href="https://greenmedinfo.com/article/ginsenoside-rg1-protects-against-sepsis-associated-encephalopathy" target="_blank">read more</a></p> https://greenmedinfo.com/article/ginsenoside-rg1-protects-against-sepsis-associated-encephalopathy#comments Encephalopathy Ginsenosides Sepsis Anti-Apoptotic Neuroprotective Agents Animal Study Fri, 28 Dec 2018 03:48:13 +0000 greenmedinfo 176557 at https://greenmedinfo.com Hydrogen water reduces NSE, IL-6, and TNF-α levels in hypoxic-ischemic encephalopathy. https://greenmedinfo.com/article/hydrogen-water-reduces-nse-il-6-and-tnf-levels-hypoxic-ischemic-encephalopathy PMID:  Open Med (Wars). 2016 ;11(1):399-406. Epub 2016 Oct 21. PMID: 28352827 Abstract Title:  Hydrogen water reduces NSE, IL-6, and TNF-αlevels in hypoxic-ischemic encephalopathy. Abstract:  This study retrospectively analyzed the efficacy of hydrogen water in the treatment of neonatal hypoxic-ischemic encephalopathy (HIE) and its effect on serum neuron-specific enolase (NSE), interleukin-6 (IL-6), and tumor necrosis factor-α(TNF-α) levels. Forty newborns with HIE who received treatment from April 2014 to April 2015 were divided into a conventional care group and a hydrogen water group according to the different treatment methods applied. Twenty healthy full-term newborns comprised the control group. In the hydrogen water group, 5-mL/kg hydrogen water was orally administered two days after birth daily for 10 days in addition to conventional treatment. After 10 days, efficacy indicators were examined in the HIE groups. The NSE, IL-6, and TNF-αlevels were compared among all three groups. The efficacy indicators were significantly lower in the hydrogen water group compared with the conventional group. Before treatment, the serum NSE, IL-6, and TNF-αlevels in the HIE groups were higher than those in the control group. After treatment, these levels in the hydrogen water group were lower than those in the conventional group. Hydrogen water lowers serum NSE, IL-6, and TNF-αlevels in HIE newborns, thereby exerting a protective effect. <p><a href="https://greenmedinfo.com/article/hydrogen-water-reduces-nse-il-6-and-tnf-levels-hypoxic-ischemic-encephalopathy" target="_blank">read more</a></p> https://greenmedinfo.com/article/hydrogen-water-reduces-nse-il-6-and-tnf-levels-hypoxic-ischemic-encephalopathy#comments Encephalopathy Hydrogen Water Anti-Inflammatory Agents Interleukin-6 Downregulation Tumor Necrosis Factor (TNF) Alpha Inhibitor Human Study Sat, 23 Mar 2024 19:53:51 +0000 greenmedinfo 291961 at https://greenmedinfo.com Icariin could attenuate AGE-induced oxidative stress and mitochondrial apoptosis. https://greenmedinfo.com/article/icariin-could-attenuate-age-induced-oxidative-stress-and-mitochondrial-apoptos PMID:  Oxid Med Cell Longev. 2019 ;2019:7940808. Epub 2019 Apr 22. PMID: 31178973 Abstract Title:  Icariin Inhibits AGE-Induced Injury in PC12 Cells by Directly Targeting Apoptosis Regulator Bax. Abstract:  Diabetic encephalopathy (DE) is a serious complication caused by long-term cognitive impairment in diabetic patients. At present, there is no effective treatment for DE. Icariin (ICA) is a bioactive ingredient isolated from. Previous research indicated that ICA was neuroprotective against A-induced PC12 cell insult; however, the effect of ICA on an advanced glycosylation end product- (AGE-) induced neural injury model has not been studied. In this study, we investigated the neuroprotective effects of ICA on AGE-induced injury in PC12 cells. Our findings revealed that ICA could effectively protect PC12 cells from AGE-induced cell apoptosis by suppressing oxidative stress. Moreover, we observed that ICA could significantly protect against mitochondrial depolarization following AGE stimulation and inactivate the mitochondria-dependent caspase-9/3 apoptosis pathway. Most notably, we identified the direct target protein of ICA as apoptosis regulator Bax by a pulldown assay. We found that ICA could specifically target Bax protein and inhibit Bax dimer formation and migration to mitochondria. Furthermore, a siRNA knockdown experiment revealed that ICA could inhibit PC12 cell apoptosis and oxidative stress through targeting Bax. Taken together, our findings demonstrated that ICA could attenuate AGE-induced oxidative stress and mitochondrial apoptosis by specifically targeting Bax and further regulating the biological function of Bax on mitochondria. <p><a href="https://greenmedinfo.com/article/icariin-could-attenuate-age-induced-oxidative-stress-and-mitochondrial-apoptos" target="_blank">read more</a></p> https://greenmedinfo.com/article/icariin-could-attenuate-age-induced-oxidative-stress-and-mitochondrial-apoptos#comments Advanced Glycation End products (AGE) Diabetes: Cognitive Dysfunction Encephalopathy Flavonoids Icariin Anti-Apoptotic Antioxidants Neuroprotective Agents In Vitro Study Thu, 05 May 2022 00:44:33 +0000 greenmedinfo 257200 at https://greenmedinfo.com