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کارودیلول آسیب مغزی ناشی از آکریل آمید را از طریق مهار مدیاتورهای اکسیداتیو، التهابی و آپوپتوتیک کاهش می دهد.

امیرشاهرخی, کیوان ، آبزیرکان, آرزو (1401) کارودیلول آسیب مغزی ناشی از آکریل آمید را از طریق مهار مدیاتورهای اکسیداتیو، التهابی و آپوپتوتیک کاهش می دهد. Iranian Journal of Basic Medical Sciences ــ 25 (1). ص.ص.67-60. شاپا 2008-3866

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آدرس اینترنتی رسمی : https://ijbms.mums.ac.ir/article_19400.html


عنوان انگليسی

Carvedilol attenuates acrylamide-induced brain damage through inhibition of oxidative, inflammatory, and apoptotic mediators

خلاصه انگلیسی

Objective(s): Acrylamide is a potent neurotoxic compound and has harmful effects on the brain cells. Acrylamide promotes oxidative, inflammatory and apoptotic mediators in the CNS leading to neurological disorders. The goal of the current study was to examine the potential protective effect of carvedilol and its underlying mechanisms in a mouse model of acrylamide-induced brain injury. Materials and Methods: Mice were treated with acrylamide (50 mg/kg/day, ip) and carvedilol (5 and 10 mg/kg/day, oral) for 11 continuous days. At the end of the experiment, mice were subjected to gait assessment. Mice were sacrificed and brain tissues were collected for histological and biochemical analysis. Results: The results showed that treatment of mice with carvedilol decreased acrylamide-induced body weight loss, abnormal gait and histopathological damage in the brain tissue. Carvedilol treatment significantly reduced the levels of malondialdehyde (MDA) and carbonyl protein, and increased the levels of glutathione (GSH), catalase, superoxide dismutase (SOD), nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Carvedilol treatment also decreased myeloperoxidase (MPO) activity, the expression of nuclear factor kappa B (NF-κB), inducible nitric oxide synthase (iNOS), the overproduction of nitric oxide (NO) and proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in the brain of mice exposed to acrylamide. Furthermore, administration of carvedilol significantly decreased the levels of bax, cytochrome-c and caspase-3 as markers of apoptosis in acrylamide-treated mice. Conclusion: These findings indicate that carvedilol is able to attenuate acrylamide-induced damage to the CNS by the inhibition of oxidative stress, inflammation and apoptosis.

نوع سند :مقاله
زبان سند : انگلیسی
نویسنده مسئول :کیوان امیرشاهرخی
نویسنده :آرزو آبزیرکان
ضریب تاثیر و نمایه مجلات:IF: 2.532 Indexed in: ISI, Scopus, PubMed, Embase
کلیدواژه ها (انگلیسی):Acrylamide; Carvedilol; Brain; Oxidative stress; Inflammation; Apoptosis
موضوعات :QV فارماکولوژی
بخش های دانشگاهی :دانشکده داروسازی > بخش فارماکولوژی
کد شناسایی :16004
ارائه شده توسط : دکتر کیوان امیرشاهرخی
ارائه شده در تاریخ :12 مرداد 1401 09:13
آخرین تغییر :12 مرداد 1401 09:13

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