سلیمی, احمد ، جمالی, ژاله ، شعبانی, محمد (1400) پتانسیل آنتی اکسیدانی و مهار منافذ انتقال نفوذپذیری میتوکندری توسط میرسیتین باعث کاهش سمیت سلولی ناشی از فسفید آلومینیوم و اختلالات میتوکندری می شود. Frontiers in Pharmacology ــ 12 (71908). شاپا 1663-9812
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آدرس اینترنتی رسمی : https://www.frontiersin.org/articles/10.3389/fphar...
عنوان انگليسی
Antioxidant Potential and Inhibition of Mitochondrial Permeability Transition Pore by Myricetin Reduces Aluminium Phosphide-Induced Cytotoxicity and Mitochondrial Impairments
خلاصه انگلیسی
Oxidative stress and mitochondrial dysfunction are involved in the mechanisms of cardiac toxicity induced by aluminum phosphide (AlP). AlP-induced cardiotoxicity leads to cardiomyocyte death, cardiomyopathy, cardiac dysfunction, and eventually severe heart failure and death. Importantly, protecting cardiomyocytes from death resulting from AlP is vital for improving survival. It has been reported that flavonoids such as myricetin (Myr) act as modifiers of mitochondrial function and prevent mitochondrial damage resulting from many insults and subsequent cell dysfunction. In this study, the ameliorative effect of Myr, as an important antioxidant and mitochondrial protective agent, was investigated in cardiomyocytes and mitochondria isolated from rat heart against AlP-induced toxicity, oxidative stress, and mitochondrial dysfunction. Treatment of AlP (20 μg/ml) significantly increased cytotoxicity; reduced glutathione (GSH) depletion, cellular reactive oxygen species (ROS) formation, malondialdehyde (MDA) level, ATP depletion, caspase-3 activation, mitochondrial membrane potential (ΔΨm) collapse, and lysosomal dysfunction; and decreased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in intact cardiomyocytes. Also, treatment of AlP (20 μg/ml) significantly increased mitochondrial dysfunction and swelling in isolated mitochondria. Myr (80 µM) appeared to ameliorate AlP-induced cytotoxicity in isolated cardiomyocytes; significantly lessened the AlP-stimulated intracellular ROS and MDA production and depletion of GSH; and increased the activities of SOD, CAT, and GSH-Px. Furthermore, Myr (40 and 80 µM) lowered AlP-induced lysosomal/mitochondrial dysfunction, ATP depletion, and caspase-3 activation. In the light of these findings, we concluded that Myr through antioxidant potential and inhibition of mitochondrial permeability transition (MPT) pore exerted an ameliorative role in AlP-induced toxicity in isolated cardiomyocytes and mitochondria, and it would be valuable to examine its in vivo effects.
نوع سند : | مقاله |
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زبان سند : | انگلیسی |
نویسنده مسئول : | احمد سلیمی |
نویسنده : | ژاله جمالی |
نویسنده : | محمد شعبانی |
ضریب تاثیر و نمایه مجلات: | IF: 5.811 Indexed in: ISI, Scopus, PubMed/PMC, Embase |
کلیدواژه ها (فارسی): | کاردیومیوپاتی، مسمومیت، فلاونوئیدها، آنتی اکسیدان ها، اختلال عملکرد میتوکندری |
کلیدواژه ها (انگلیسی): | Cardiomyopathy, Poisoning, Flavonoids, Antioxidant, Mitochondrial Dysfunction |
موضوعات : | QV فارماکولوژی > QV 600 سم شناسی QV فارماکولوژی |
بخش های دانشگاهی : | دانشکده داروسازی > بخش سم شناسی |
کد شناسایی : | 14875 |
ارائه شده توسط : | دکتر احمد سلیمی |
ارائه شده در تاریخ : | 21 آذر 1400 12:18 |
آخرین تغییر : | 25 فروردین 1401 09:16 |
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