Anti-Apoptotic https://greenmedinfo.com/category/keywords/Anti-Apoptotic en Administration of deep sea minerals can be an effective strategy to improve the life expectancy of diabetic subjects. https://greenmedinfo.com/article/administration-deep-sea-minerals-can-be-effective-strategy-improve-life-expect n/a PMID:  Environ Toxicol. 2016 Jul ;31(7):769-81. Epub 2015 Mar 2. PMID: 25727812 Abstract Title:  Deep sea minerals prolong life span of streptozotocin-induced diabetic rats by compensatory augmentation of the IGF-I-survival signaling and inhibition of apoptosis. Abstract:  Consumption of deep sea minerals (DSM), such as magnesium, calcium, and potassium, is known to reduce hypercholesterolemia-induced myocardial hypertrophy and cardiac-apoptosis and provide protection against cardiovascular diseases. Heart diseases develop as a lethal complication among diabetic patients usually due to hyperglycemia-induced cardiac-apoptosis that causes severe cardiac-damages, heart failure, and reduced life expectancy. In this study, we investigated the potential of DSM and its related cardio-protection to increase the life expectancy in diabetic rats. In this study, a heart failure rat model was developed by using streptozotocin (65 mg kg(-1) ) IP injection. Different doses of DSM-1× (37 mg kg(-1) day(-1) ), 2× (74 mg kg(-1) day(-1) ) and 3× (111 mg kg(-1) day(-1) ), were administered to the rats through gavages for 4 weeks. The positive effects of DSM on the survival rate of diabetes rats were determined with respect to the corresponding effects of MgSO4 . Further, to understand the mechanism by which DSM enhances the survival of diabetic rats, their potential to regulate cardiac-apoptosis and control cardiac-dysfunction were examined. Echocardiogram, tissue staining, TUNEL assay, and Western blotting assay were used to investigate modulations in the myocardial contractile function and related signaling protein expression. The results showed that DSM regulate apoptosis and complement the cardiomyocyte proliferation by enhancing survival mechanisms. Moreover DSM significantly reduced the mortality rate and enhanced the survival rate of diabetic rats. Experimental results show that DSM administration can be an effective strategy to improve the life expectancy of diabetic subjects by improving cardiac-cell proliferation and by controlling cardiac-apoptosis and associated cardiac-dysfunction. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 769-781, 2016. https://greenmedinfo.com/article/administration-deep-sea-minerals-can-be-effective-strategy-improve-life-expect#comments Diabetic Complications Heart Failure Water: Deep Sea Anti-Apoptotic Cardioprotective Anti-Apoptotic Cardioprotective Diabetic Complications Heart Failure Water: Deep Sea Animal Study Mon, 03 Apr 2017 17:19:20 +0000 greenmedinfo 145829 at https://greenmedinfo.com Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction. https://greenmedinfo.com/article/allicin-improves-cardiac-function-protecting-against-apoptosis-rat-model-myoca n/a PMID:  Chin J Integr Med. 2017 Aug ;23(8):589-597. Epub 2016 Jul 13. PMID: 27412589 Abstract Title:  Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction. Abstract:  OBJECTIVE: To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI). METHODS: Ninety-four Wistar rats were randomly assigned to 6 groups (n=14-16 per group): sham control group [underwent thoracotomy without left anterior descending (LAD) occlusion and only received an injection of the same amount of citrate buffer], MI control group (subjected to LAD occlusion and only received an injection of same amount of citrate buffer), positive control group (subjected to LAD occlusion and received an injection of diltiazem hydrochloride at the dose of 1.5 mg/kg), and MI + allicin groups (subjected to LAD occlusion and received an injection of allicin at the doses of 1.2, 1.8, and 3.6 mg/kg). All of the drugs were administered intraperitoneally daily for 21 days. The infarct area was measured by myocardial staining. Hematoxylin-eosin staining was used to observe the pathological changes. Cardiac function parameters were assessed by echocardiography. The myocardial apoptotic index was estimated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining. The expression of Bax and Bcl-2 were detected by quantificational real-time polymerase chain reaction and Western blot. RESULTS: Treatment with allicin could attenuate the myocardial infarct area (P<0.05) and relieve the changes of the myocardium. The left ventricular anterior wall diastolic and systolic thicknesses were increased in the allicin-treated groups (P<0.05), while there was no signifificant difference in the left ventricular posterior wall diastolic and systolic thickness (P>0.05). The left ventricular internal diameter in systole, ejection fraction, fractional shortening, and stroke volume were dramatically elevated in allicin-treated rats (P<0.05). Allicin dose-dependently reduced creatine kinase and lactate dehydrogenase levels (P<0.05). The myocardial apoptotic index was also markedly lowered, and Bax expression was signifificantly decreased, whereas Bcl-2 expression exhibited an opposite trend in allicin-treated rats (P<0.05). CONCLUSION: Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis, further improving cardiac function. https://greenmedinfo.com/article/allicin-improves-cardiac-function-protecting-against-apoptosis-rat-model-myoca#comments Allicin Myocardial Infarction Anti-Apoptotic Cardioprotective Allicin Anti-Apoptotic Cardioprotective Myocardial Infarction Animal Study Thu, 07 Sep 2017 23:10:09 +0000 greenmedinfo 152928 at https://greenmedinfo.com Chrysin possesses restorative effect against paracetamol induced hepatotoxicity. https://greenmedinfo.com/article/chrysin-possesses-restorative-effect-against-paracetamol-induced-hepatotoxicit n/a PMID:  J Biochem Mol Toxicol. 2017 Nov ;31(11). Epub 2017 Jul 6. PMID: 28682524 Abstract Title:  Restorative effects of Chrysin pretreatment on oxidant-antioxidant status, inflammatory cytokine production, and apoptotic and autophagic markers in acute paracetamol-induced hepatotoxicity in rats: An experimental and biochemical study. Abstract:  Paracetamol (PC) is a widely used analgesic and antipyretic drug, but it leads to acute hepatotoxicity at high doses intakes. This study was aimed to investigate the effects of Chrysin (CR) on hepatotoxicity constituted at high doses of PC in rats. Rats were subjected to oral pretreatment of CR (25 and 50 mg/kg b.w.) via feeding needle for 6 days against hepatotoxicity induced by a single dose of PC (500 mg/kg b.w.) administered orally via feeding needles. Although PC increases lipid peroxidation and liver enzyme activities, it has led to reduction of antioxidant enzyme activities. PC induced inflammatory responses by increasing the levels of TNF-α and IL-1β. Furthermore, PC caused apoptosis and autophagy by increasing activity of Caspase-3 and LC3B level. On the other hand, CR therapy significantly regulated these values in rats. This study demonstrated that CR possesses restorative effect against PC-induced hepatotoxicity by suppressing oxidative stress, inflammation, and apoptotic and autophagic tissue damage. https://greenmedinfo.com/article/chrysin-possesses-restorative-effect-against-paracetamol-induced-hepatotoxicit#comments Acetaminophen (Tylenol) Toxicity Chrysin Lipid Peroxidation Acetaminophen Anti-Apoptotic Antioxidants Hepatoprotective Paracetamol Acetaminophen (Tylenol) Toxicity Anti-Apoptotic Antioxidants Chrysin Hepatoprotective Lipid Peroxidation Animal Study Thu, 08 Feb 2018 03:51:48 +0000 greenmedinfo 159488 at https://greenmedinfo.com Diallyl trisulfide suppresses oxidative stress-induced activation of hepatic stellate cells. https://greenmedinfo.com/article/diallyl-trisulfide-suppresses-oxidative-stress-induced-activation-hepatic-stel n/a PMID:  Oxid Med Cell Longev. 2017 ;2017:1406726. Epub 2017 Feb 20. PMID: 28303169 Abstract Title:  Diallyl Trisulfide Suppresses Oxidative Stress-Induced Activation of Hepatic Stellate Cells through Production of Hydrogen Sulfide. Abstract:  Accumulating data reveal that garlic has beneficial effects against chronic liver disease. We previously reported that diallyl trisulfide (DATS), the primary organosulfur compound in garlic, reduced fibrosis and attenuated oxidative stress in rat fibrotic liver. The present study was aimed at elucidating the underlying mechanisms. The primary rat hepatic stellate cells (HSCs) were cultured and stimulated with hydrogen peroxide (H2O2) for inducing HSC activation under oxidative stress. We examined the effects of DATS on the profibrogenic properties and oxidative stress in H2O2-treated HSCs. The results showed that DATS suppressed and reduced fibrotic marker expression in HSCs. DATS arrested cell cycle at G2/M checkpoint associated with downregulating cyclin B1 and cyclin-dependent kinase 1, induced caspase-dependent apoptosis, and reduced migration in HSCs. Moreover, intracellular levels of reactive oxygen species and lipid peroxide were decreased by DATS, but intracellular levels of glutathione were increased in HSCs. Furthermore, DATS significantly elevated hydrogen sulfide (H2S) levels within HSCs, but iodoacetamide (IAM) reduced H2S levels and significantly abrogated DATS production of H2S within HSCs. IAM also abolished all the inhibitory effects of DATS on the profibrogenic properties and oxidative stress in HSCs. Altogether, we demonstrated an H2S-associated mechanism underlying DATS inhibition of profibrogenic properties and alleviation of oxidative stress in HSCs. Modulation of H2S production may represent a therapeutic remedy for liver fibrosis. https://greenmedinfo.com/article/diallyl-trisulfide-suppresses-oxidative-stress-induced-activation-hepatic-stel#comments Garlic Liver Cirrhosis Oxidative Stress Anti-Apoptotic Antioxidants Anti-Apoptotic Antioxidants Garlic Liver Cirrhosis oxidative stress Animal Study Tue, 11 Apr 2017 20:17:31 +0000 greenmedinfo 146158 at https://greenmedinfo.com Eugenol holds potential as a neuroprotective agent against aluminium induced brain toxicity. https://greenmedinfo.com/article/eugenol-holds-potential-neuroprotective-agent-against-aluminium-induced-brain- n/a PMID:  Arh Hig Rada Toksikol. 2017 Mar 1 ;68(1):27-37. PMID: 28365674 Abstract Title:  Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain. Abstract:  Aluminium (Al) is a neurotoxic metal that contributes to the progression of several neurodegenerative diseases. The aim of the present study was to evaluate the protective effect of dietary eugenol supplementation against aluminium (Al)- induced cerebral damage in rats. Male Wistar rats were divided into four groups: normal controls, rats fed a diet containing 6,000μg g-1 eugenol, rats intoxicated daily with aluminium chloride (84 mg kg-1 body weight) p. o. and fed either a basal diet or a eugenol-containing diet. Daily oral administration of Al for four consecutive weeks to rats significantly reduced brain total antioxidant status (TAS) (11.42±0.31 μmol g-1 tissue, p<0.001) with a subsequent significant enhancement of lipid peroxidation (MDA) (32.55±1.68 nmol g-1 tissue, p<0.002). In addition, Al enhanced brain acetylcholinesterase activity (AChE) (46.22±4.90 U mg-1 protein, p<0.001), tumour necrosis factor alpha (TNF-α) (118.72±11.32 pg mg-1 protein, p<0.001), and caspase 3 (Casp-3) (8.77±1.26 ng mg-1 protein, p<0.001) levels, and in contrast significantly suppressed brain-derived neurotrophic factor (BDNF) (82.74±14.53 pg mg-1 protein, p<0.002) and serotonin (5-HT) (1.54±0.12 ng mg-1 tissue, p<0.01) levels. Furthermore, decreased glial fibrillary acidic protein (GFAP) immunostaining was noticed in the striatum of Al-intoxicated rats, compared with untreated controls. On the other hand, co-administration of dietary eugenol with Al intoxication restored brain BDNF (108.76±2.64 pg mg-1 protein) and 5-HT (2.13±0.27 ng mg-1 tissue) to normal levels, enhanced brain TAS (13.43±0.24 μmol g-1 tissue, p<0.05), with a concomitant significant reduction in TNF-α (69.98±4.74 pg mg-1 protein) and Casp-3 (3.80±0.37 ng mg-1 protein) levels (p<0.001), as well as AChE activity (24.50±3.25 U mg-1 protein, p<0.001), and increased striatal GFAP immunoreactivity, compared with Al-treated rats. Histological findings of brain tissues verified biochemical data. In conclusion, eugenol holds potential as a neuroprotective agent through its hydrophobic, antioxidant, and anti-apoptotic properties, as well as its neurotrophic ability against Al-induced brain toxicity in rats. https://greenmedinfo.com/article/eugenol-holds-potential-neuroprotective-agent-against-aluminium-induced-brain-#comments Aluminum Toxicity Eugenol Aluminum Chloride Anti-Apoptotic Antioxidants Neuroprotective Agents aluminum toxicity Anti-Apoptotic Antioxidants eugenol Neuroprotective Agents Animal Study Mon, 10 Apr 2017 13:24:48 +0000 greenmedinfo 146101 at https://greenmedinfo.com M. alba has protective effect on diabetic retinopathy. https://greenmedinfo.com/article/m-alba-has-protective-effect-diabetic-retinopathy n/a PMID:  Eur J Nutr. 2016 Apr 8. Epub 2016 Apr 8. PMID: 27059477 Abstract Title:  Consumption of polyphenol-rich Morus alba leaves extract attenuates early diabetic retinopathy: the underlying mechanism. Abstract:  PURPOSE: Beneficial effects of white mulberry against diabetes mellitus have been reported. However, the molecular mechanisms of how white mulberry can attenuate diabetic retinopathy remain poorly understood. Here, the mechanism underlying the protective effect of Morus alba leaves ethanolic extract on oxidative stress, inflammation, apoptosis, and angiogenesis in diabetic retinopathy was investigated. METHODS: Diabetes was induced by injection of streptozotocin. One week after, M. alba (100 mg/kg) was administrated to the rats daily for 16 weeks. RESULTS: Morus alba extract showed high content of polyphenolics and free radical scavenging activity. Oral M. alba administration significantly attenuated hyperglycemia and weight loss, and decreased sorbitol, fructose, protein kinase C, pro-inflammatory cytokines, and oxidative stress markers in retinas of the diabetic rats. Moreover, M. alba produced marked down-regulation of caspase-3 and Bax, with concomitant up-regulation of Bcl-2 in the diabetic retinas. M. alba also reduced the expression of VEGF in the retina. CONCLUSION: These results indicate that M. alba has protective effect on diabetic retinopathy with possible mechanisms of inhibiting hyperglycemia-induced oxidative stress, apoptosis, inflammation, polyol pathway activation, and VEGF expression in the retina. https://greenmedinfo.com/article/m-alba-has-protective-effect-diabetic-retinopathy#comments Diabetic Retinopathy White Mulberry Anti-Apoptotic Anti-Inflammatory Agents Hypoglycemic Agents Vascular Endothelial Growth Factor Inhibitors Anti-Apoptotic Anti-Inflammatory Agents Diabetic Retinopathy Hypoglycemic Agents Vascular Endothelial Growth Factor Inhibitors White Mulberry Animal Study Wed, 22 Feb 2017 17:47:48 +0000 greenmedinfo 143855 at https://greenmedinfo.com Mangiferin induces islet regeneration in aged mice. https://greenmedinfo.com/article/mangiferin-induces-islet-regeneration-aged-mice n/a PMID:  Int J Mol Med. 2018 Mar 1. Epub 2018 Mar 1. PMID: 29512742 Abstract Title:  Mangiferin induces islet regeneration in aged mice through regulating p16INK4a. Abstract:  Previous studies by our group on mangiferin demonstrated that it exerts an anti‑hyperglycemic effect through the regulation of cell cycle proteins in 3‑month‑old, partially pancreatectomized (PPx) mice. However, β‑cell proliferation is known to become severely restricted with advanced age. Therefore, it is unknown whether mangiferin is able to reverse the diabetic condition and retain β‑cell regeneration capability in aged mice. In the present study, 12‑month‑old C57BL/6J mice that had undergone PPx were subjected to mangiferin treatment (90 mg/kg) for 28 days. Mangiferin‑treated aged mice exhibited decreased blood glucose levels and increased glucosetolerance, which was accompanied with higher serum insulin levels when compared with those in untreated PPx control mice. In addition, islet hyperplasia, elevated β‑cell proliferation and reduced β‑cell apoptosis were also identified in the mice that received mangiferin treatment. Further studies on the mRNA transcript and protein expression levels indicated comparatively increased levels of cyclins D1 and D2 and cyclin‑dependent kinase 4 in mangiferin‑treated mice, while the levels of p27Kip1 and p16INK4a were decreased relative to those in the untreated PPx controls. Of note, mangiferin treatment improved the proliferation rate of islet β‑cells in adult mice overexpressing p16INK4a, suggesting that mangiferin induced β‑cell proliferation via the regulation of p16INK4a. In addition, the mRNA transcription levels of critical genes associated with insulin secretion, including pancreatic and duodenal homeobox 1, glucose transporter 2 and glucokinase, were observed to be upregulated after mangiferin treatment. Taken together, it was indicated that mangiferin treatment significantly induced β‑cell proliferation and inhibited β‑cell apoptosis by regulating cell cycle checkpoint proteins. Furthermore, mangiferin was also demonstrated to regulate genes associated with insulin secretion. Collectively these, results suggest the therapeutic potential of mangiferin in the treatment of diabetes in aged individuals. https://greenmedinfo.com/article/mangiferin-induces-islet-regeneration-aged-mice#comments Mangiferin Anti-Apoptotic Pancreato Protective Agents Anti-Apoptotic Mangiferin Pancreato Protective Agents Animal Study Sat, 10 Mar 2018 03:48:58 +0000 greenmedinfo 161009 at https://greenmedinfo.com Melatonin promotes brain-derived neurotrophic factor expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia. https://greenmedinfo.com/article/melatonin-promotes-brain-derived-neurotrophic-factor-expression-and-anti-apopt n/a PMID:  Med Sci Monit. 2017 Dec 16 ;23:5951-5959. Epub 2017 Dec 16. PMID: 29247156 Abstract Title:  Melatonin Promotes Brain-Derived Neurotrophic Factor (BDNF) Expression and Anti-Apoptotic Effects in Neonatal Hemolytic Hyperbilirubinemia via a Phospholipase (PLC)-Mediated Mechanism. Abstract:  BACKGROUND Melatonin therapy shows positive effects on neuroprotective factor brain-derived neurotrophic factor (BDNF) expression and neuronal apoptosis in neonatal hemolytic hyperbilirubinemia. We hypothesized that melatonin promotes BDNF expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia through a phospholipase (PLC)-mediated mechanism. MATERIAL AND METHODS A phenylhydrazine hydrochloride (PHZ)-induced neonatal hemolytic hyperbilirubinemia model was constructed in neonatal rats. Four experimental groups - a control group (n=30), a PHZ group (n=30), a PHZ + melatonin group (n=30), and a PHZ + melatonin+U73122 (a PLC inhibitor) group (n=30) - were constructed. Trunk blood was assayed for serum hemoglobin, hematocrit, total and direct bilirubin, BDNF, S100B, and tau protein levels. Brain tissue levels of neuronal apoptosis, BDNF expression, PLC activity, IP3 content, phospho- and total Ca2+/calmodulin-dependent protein kinase type IV (CaMKIV) expression, and phospho- and total cAMP response element binding protein (CREB) expression were also assayed. RESULTS PHZ-induced hemolytic hyperbilirubinemia was validated by significantly decreased serum hemoglobin and hematocrit as well as significantly increased total and direct serum bilirubin (p<0.05). Neonatal bilirubin-induced neurotoxicity was validated by significantly decreased serum BDNF, brain BDNF, and serum S100B, along with significantly increased serum tau protein (p<0.05). PHZ-induced hemolytic hyperbilirubinemia significantly decreased serum BDNF, brain BDNF, and PLC/IP3/Ca2+ pathway activation while increasing neuronal apoptosis levels (p<0.05), all of which were partially rescued by melatonin therapy (p<0.05). Pre-treatment with the PLC inhibitor U73122 largely abolished the positive effects of melatonin on PLC/IP3/Ca2+ pathway activation, downstream BDNF levels, and neuronal apoptosis (p<0.05). CONCLUSIONS Promotion of BDNF expression and anti-apoptotic effects in neonatal hemolytic hyperbilirubinemia by melatonin largely operates via a PLC-mediated mechanism. https://greenmedinfo.com/article/melatonin-promotes-brain-derived-neurotrophic-factor-expression-and-anti-apopt#comments Hyperbilirubinemia: Hereditary Melatonin Anti-Apoptotic Brain-derived neurotrophic factor modulator Anti-Apoptotic Brain-derived neurotrophic factor modulator Hyperbilirubinemia: Hereditary melatonin Animal Study Fri, 19 Jan 2018 01:19:50 +0000 greenmedinfo 158582 at https://greenmedinfo.com Panax notoginseng saponins attenuate cardiomyocyte apoptosis through mitochondrial pathway in natural aging rats. https://greenmedinfo.com/article/panax-notoginseng-saponins-attenuate-cardiomyocyte-apoptosis-through-mitochond n/a PMID:  Phytother Res. 2018 Feb ;32(2):243-250. Epub 2017 Nov 12. PMID: 29130614 Abstract Title:  Panax notoginseng saponins attenuate cardiomyocyte apoptosis through mitochondrial pathway in natural aging rats. Abstract:  Panax notoginseng saponins (PNS) have been widely used in the cardiovascular system for the treatment of cardiovascular diseases and stroke in China. In this study, we investigated the anti-apoptotic effect of PNS on cardiomyocytes in the natural aging rat and explored the potential mechanisms regarding oxidative stress and mitochondrial function signaling pathways. Male Sprague-Dawley rats were randomly divided into five groups: adult control (3-month old), aging control (24-month old), and different doses of PNS-treated aging rat groups (10, 30, 60 mg/kg/day, orally). After treatment of PNS or saline for 6 months, the effects of PNS on the cardiomyocytes were evaluated. Results showed that PNS significantly improved the morphological changes in myocardium, prevented the increase of cardiomyocyte apoptosis in the aging rats, and improved mitochondrial dysfunction associated aging in a dose-dependent manner. PNS also significantly reversed the down-regulation of FoxO3a and Mn-SOD and up-regulated PGC-1α, LC3β, and Beclin-1 levels. Our data demonstrated that during aging, mitochondrial dysfunction caused an increase of oxidative damage, which played a key role in cardiomyocyte apoptosis. PNS exerted an anti-apoptotic effect via attenuating oxidative damage through oxidative stress- and mitochondrial function-related signaling pathways. https://greenmedinfo.com/article/panax-notoginseng-saponins-attenuate-cardiomyocyte-apoptosis-through-mitochond#comments Aging: Heart Panax Notoginseng Anti-Apoptotic Antioxidants Cardioprotective Aging: Heart Anti-Apoptotic Antioxidants Cardioprotective Panax Notoginseng Animal Study Fri, 02 Mar 2018 07:57:15 +0000 greenmedinfo 160625 at https://greenmedinfo.com Phloretin has an anti-apoptotic effect on cisplatin-induced apoptosis in HEI-OC1 auditory cells. https://greenmedinfo.com/article/phloretin-has-anti-apoptotic-effect-cisplatin-induced-apoptosis-hei-oc1-audito n/a PMID:  Pharmacol Rep. 2011 ;63(3):708-16. PMID: 21857081 Abstract Title:  Anti-apoptotic effect of phloretin on cisplatin-induced apoptosis in HEI-OC1 auditory cells. Abstract:  Cisplatin is a highly effective chemotherapeutic agent, but it has significant ototoxic side effects. Apoptosis is an important mechanism of cochlear hair cell loss following exposure to cisplatin. The present study examined the effects of phloretin, a natural polyphenolic compound found in apples and pears, on cisplatin-induced apoptosis. We found that phloretin induced the expression of heme oxygenase-1 (HO-1) protein in a concentration- and time-dependent manner. Phloretin induced nuclear factor-E2-related factor 2 (Nrf2) nuclear translocation, and dominant-negative Nrf2 attenuated phloretin-induced expression of HO-1. Phloretin activated the JNK, ERK and p38 mitogen-activated protein kinase (MAPK) pathways, and the JNK pathway played an important role in phloretin-induced HO-1 expression. Phloretin protected the cells against cisplatin-induced apoptosis. The protective effect of phloretin was abrogated by zinc protoporphyrin IX (ZnPP IX), a HO inhibitor. Furthermore, phloretin pretreatment inhibited mitochondrial dysfunction and the activation of caspases. These results demonstrate that the expression of HO-1 induced by phloretin is mediated by both the JNK pathway and Nrf2; the expression inhibits cisplatin-induced apoptosis in HEI-OC1 cells. https://greenmedinfo.com/article/phloretin-has-anti-apoptotic-effect-cisplatin-induced-apoptosis-hei-oc1-audito#comments Chemotherapy-Induced Toxicity: Cisplatin Phloretin Anti-Apoptotic Chemoprotective Agents Heme oxygenase-1 inducer Anti-Apoptotic Chemoprotective Agents Chemotherapy-Induced Toxicity: Cisplatin Heme oxygenase-1 inducer Phloretin In Vitro Study Fri, 03 Mar 2017 22:20:44 +0000 greenmedinfo 144372 at https://greenmedinfo.com Puerarin inhibited cadmium induced apoptosis in rPT cells by ameliorating the mitochondrial dysfunction. https://greenmedinfo.com/article/puerarin-inhibited-cadmium-induced-apoptosis-rpt-cells-ameliorating-mitochondr n/a PMID:  Chem Biol Interact. 2016 Dec 25 ;260:219-231. Epub 2016 Oct 4. PMID: 27717697 Abstract Title:  Puerarin protects against cadmium-induced proximal tubular cell apoptosis by restoring mitochondrial function. Abstract:  Puerarin (PU) is a potent free radical scavenger with a protective effect in nephrotoxin-mediated oxidative damage. Here, we show a novel molecular mechanism by which PU exerts its anti-apoptotic effects in cadmium (Cd)-exposed primary rat proximal tubular (rPT) cells. Morphological assessment and flow cytometric analysis revealed that PU significantly decreased Cd-induced apoptotic cell death of rPT cells. Administration of PU protected cells against Cd-induced depletion of mitochondrial membrane potential (ΔΨm) and lipid peroxidation. Cd-mediated mitochondrial permeability transition pore (MPTP) opening, disruption of mitochondrial ultrastructure, mitochondrial cytochrome c (cyt-c) release, caspase-3 activation and subsequently poly ADP-ribose polymerase (PARP) cleavage could be effectively blockedby the addition of PU. Moreover, up-regulation of Bcl-2 and down-regulation of Bax and hence increased Bcl-2/Bax ratio were observed with the PU administration. In addition, PU reversed Cd-induced ATP depletion by restoring ΔΨm to affect ATP production and by regulating expression levels of ANT-1and ANT-2 to improve ATP transport. In summary, PU inhibited Cd-induced apoptosis in rPT cells by ameliorating the mitochondrial dysfunction. https://greenmedinfo.com/article/puerarin-inhibited-cadmium-induced-apoptosis-rpt-cells-ameliorating-mitochondr#comments Cadmium Poisoning Puerarin Anti-Apoptotic Bax/Bcl2 ratio: Increase Cadmium Anti-Apoptotic Bax/Bcl2 Cadmium Cadmium Poisoning Puerarin In Vitro Study Fri, 02 Dec 2016 21:46:48 +0000 greenmedinfo 139813 at https://greenmedinfo.com Shikonin attenuated hepatic ischemia/reperfusion injury by inhibiting apoptosis and autophagy. https://greenmedinfo.com/article/shikonin-attenuated-hepatic-ischemiareperfusion-injury-inhibiting-apoptosis-an n/a PMID:  Sci Rep. 2017 Mar 21 ;7:44785. Epub 2017 Mar 21. PMID: 28322249 Abstract Title:  The protective effects of shikonin on hepatic ischemia/reperfusion injury are mediated by the activation of the PI3K/Akt pathway. Abstract:  Hepatic ischemia/reperfusion (I/R) injury, which can result in severe liver injury and dysfunction, occurs in a variety of conditions such as liver transplantation, shock, and trauma. Cell death in hepatic I/R injury has been linked to apoptosis and autophagy. Shikonin plays a significant protective role in ischemia/reperfusion injury. The purpose of the present study was to investigate the protective effect of shikonin on hepatic I/R injury and explore the underlying mechanism. Mice were subjected to segmental (70%) hepatic warm ischemia to induce hepatic I/R injury. Two doses of shikonin (7.5 and 12.5 mg/kg) were administered 2 h before surgery. Balb/c mice were randomly divided into four groups: normal control, I/R, and shikonin preconditioning at two doses (7.5 and 12.5 mg/kg). The serum and liver tissues were collected at three time points (3, 6, and 24 h). Shikonin significantly reduced serum AST and ALT levels and improved pathological features. Shikonin affected the expression of Bcl-2, Bax, caspase 3, caspase 9, Beclin-1, and LC3, and upregulated PI3K and p-Akt compared with the levels in the I/R group. Shikonin attenuated hepatic I/R injury by inhibiting apoptosis and autophagy through a mechanism involving the activation of PI3K/Akt signaling. https://greenmedinfo.com/article/shikonin-attenuated-hepatic-ischemiareperfusion-injury-inhibiting-apoptosis-an#comments Liver Injury: Ischemia/reperfusion Shikonin Anti-Apoptotic Autophagy Inhibitors Hepatoprotective Anti-Apoptotic Autophagy Inhibitors Hepatoprotective Liver Injury: Ischemia/reperfusion Shikonin Animal Study Wed, 03 May 2017 15:54:01 +0000 greenmedinfo 147166 at https://greenmedinfo.com The flavonoid glycoside astragalin may be a new therapeutic agent for the management of menopausal symptoms. https://greenmedinfo.com/article/flavonoid-glycoside-astragalin-may-be-new-therapeutic-agent-management-menopau n/a PMID:  Molecules. 2016 May 21 ;21(5). Epub 2016 May 21. PMID: 27213327 Abstract Title:  Astragalin, a Flavonoid from Morus alba (Mulberry) Increases Endogenous Estrogen and Progesterone by Inhibiting Ovarian Granulosa Cell Apoptosis in an Aged Rat Model of Menopause. Abstract:  BACKGROUND: To determine the mechanism by which the flavonoid glycoside astragalin (AST) reduces ovarian failure in an aged rat model of menopause. METHODS: The in vivo effect of AST on granulosa cell (GC) apoptosis in aged female rats was determined using flow cytometry. In vitro, the effects of AST on cultured GCs were investigated using the MTT proliferation assay and western blot assays. RESULTS: Aged rats had significantly higher GC apoptosis as compared with young female rats. Treatment of aged rats with AST (all three doses; p<0.01) or Progynova (p<0.01) significantly reduced GC apoptosis as compared with the aged controls. The proportions of total apoptotic GCs was 25.70%, 86.65%, 47.04%, 27.02%, 42.09% and 56.42% in the normal, aged, 17β-estradiol (E₂), high dose AST, medium dose AST, and low dose AST-treated groups, respectively. Significant increases of serum E₂ and P₄ levels, as well as altered levels of serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) levels. In cultured rat GCs, AST stimulated GC proliferation, E₂ and progesterone (P₄) secretion, reduced apoptosis, reduced the level of the pro-apoptotic protein Bcl-2 (p<0.01), but had no effect on BAX. CONCLUSIONS: AST enhanced ovarian function in aged female rats by increasing E₂ and P₄ levels, and reducing ovarian GC apoptosis via a mechanism involving Bcl-2. These data demonstrate a new pharmacological activity for AST, as well as a novel mechanism of action, and further suggest that AST may be a new therapeutic agent for the management of menopausal symptoms. https://greenmedinfo.com/article/flavonoid-glycoside-astragalin-may-be-new-therapeutic-agent-management-menopau#comments Flavonoids Menopausal Syndrome White Mulberry Anti-Apoptotic Anti-Apoptotic Flavonoids Menopausal Syndrome White Mulberry Animal Study Wed, 22 Feb 2017 01:13:50 +0000 greenmedinfo 143839 at https://greenmedinfo.com These findings indicate hepatic protective effects of deep sea water on diabetes mellitus. https://greenmedinfo.com/article/these-findings-indicate-hepatic-protective-effects-deep-sea-water-diabetes-mel n/a PMID:  Chin J Physiol. 2015 Jun 30 ;58(3):197-205. PMID: 26014125 Abstract Title:  Attenuated Effects of Deep-Sea Water on Hepatic Apoptosis in STZ-Induced Diabetic Rats. Abstract:  Diabetes mellitus (DM) is a metabolic disorder and increasing evidences have indicated a connection between DM and hepatic abnormality. Deep-sea water (DSW) has been applied in many fields, especially in medicine; herein, we investigated the influence of DSW on hepatic apoptosis in streptozocin (STZ)-induced diabetes rats. Our experimental results firstly demonstrated the beneficial effects of 1×DSW, 2×DSW and 3×DSW in alleviating hepatic apoptosis in STZ-induced diabetic rats. We demonstrated that 1×DSW, 2×DSW and 3×DSW significantly suppressed the caspase-3 activity and TUNEL-positive cells in livers of STZ-induced diabetic rats. Significant reductions of both Fas-dependent and mitochondrial-dependent apoptotic molecules were also detected in livers of STZ-induced diabetic rats receiving DSW. Additionally, apoptotic signaling molecules such as phosphorylated IκB-α and NF-κB were significantly reduced in livers of DSW-treated STZ-induced diabetic rats. These findings indicate hepatic protective effects of DSW on DM and suggest DSW as a possible ingredient for health food. https://greenmedinfo.com/article/these-findings-indicate-hepatic-protective-effects-deep-sea-water-diabetes-mel#comments Diabetic Complications Water: Deep Sea Anti-Apoptotic Hepatoprotective Anti-Apoptotic Diabetic Complications Hepatoprotective Water: Deep Sea Animal Study Mon, 03 Apr 2017 17:05:44 +0000 greenmedinfo 145824 at https://greenmedinfo.com These results demonstrat the radioprotective effect of folic acid supplementation on low dose ionizing radiation-induced genomic instability in vitro. https://greenmedinfo.com/article/these-results-demonstrat-radioprotective-effect-folic-acid-supplementation-low n/a PMID:  Indian J Exp Biol. 2016 08 ;54(8):537-43. PMID: 28577512 Abstract Title:  Possible radioprotective effect of folic acid supplementation on low dose ionizing radiation-induced genomic instability in vitro. Abstract:  Ionizing radiation (IR) induces DNA damage through production of single and double-strand breaks and reactive oxygen species (ROS). Folic acid (FA) prevents radiation-induced DNA damage by modification of DNA synthesis and/or repair and as a radical scavenger. We hypothesized that in vitro supplementation with FA will decrease the sensitivity of cells to genetic damage induced by low dose of ionizing radiation. Annexin V, comet and micronucleus assays were performed in cultured CHO cells. After 7 days of pre-treatment with 0, 100, 200 or 300 nM FA, cultures were exposed to radiation (100 mSv). Two un-irradiated controls were executed (0 and 100 nM FA). Data were statistically analyzed with X2-test and linear regression analysis (P0.05). We observed a significantly decreased frequency of apoptotic cells with the increasing FA concentration (P<0.05). The same trend was observed when analyzing DNA damage and chromosomal instability (P<0.05 for 300 nM). Only micronuclei frequencies showed significant differences for linear regression analysis (R2=94.04; P<0.01). Our results have demonstrated the radioprotective effect of folic acid supplementation on low dose ionizing radiation-induced genomic instability in vitro; folate status should be taken into account when studying the effect of low dose radiation in environmental or occupational exposure. https://greenmedinfo.com/article/these-results-demonstrat-radioprotective-effect-folic-acid-supplementation-low#comments DNA damage Folic Acid Anti-Apoptotic Low Dose Ionizing Radiation Radioprotective Anti-Apoptotic DNA damage folic acid Radioprotective In Vitro Study Wed, 05 Jul 2017 23:23:44 +0000 greenmedinfo 150102 at https://greenmedinfo.com