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Noori Tayebeh Shirooie Samira Sureda Antoni Sobarzo-Sanchez Eduardo Dehpour Ahmad Reza Saldías Marianela Akkol Esra Küpeli 《Neurochemical research》2022,47(8):2142-2157
Neurochemical Research - Stroke is a sudden neurological disorder that occurs due to impaired blood flow to an area of the brain. Stroke can be caused by the blockage or rupture of a blood vessel... 相似文献
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Seyed Fazel Nabavi Antoni Sureda Ahmad Reza Dehpour Samira Shirooie Ana Sanches Silva Kasi Pandima Devi Touqeer Ahmed Nafeesa Ishaq Rabia Hashim Eduardo Sobarzo-Sánchez Maria Daglia Nady Braidy Mariateresa Volpicella Rosa Anna Vacca Seyed Mohammad Nabavi 《Biotechnology advances》2018,36(6):1768-1778
In the present paper, we will discuss on the importance of autophagy in the central nervous system, and outline the relation between autophagic pathways and the pathogenesis of neurodegenerative disorders. The potential therapeutic benefits of naturally occurring phytochemicals as pharmacological modulators of autophagy will also be addressed. Our findings provide renewed insight on the molecular modes of protection by polyphenols, which is likely to be at least in part mediated not only by their potent antioxidant and anti-inflammatory effects, but also through modulation of autophagic processes to remove the aberrant protein aggregates. 相似文献
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Samira Shirooie Mousa Sahebgharani Jamileh Esmaeili Ahmad Reza Dehpour 《Journal of cellular physiology》2019,234(3):3058-3066
The chronic use of opioids leads to tolerance, psychological, and physical dependence that limits their use as an effective long-term pain control. Several studies have shown that mammalian target of rapamycin (mTOR) plays a crucial role in the development of opioid tolerance. Metformin activates 5′ adenosine monophosphate-activated protein kinase (AMPK) which directly suppresses the mTOR complex 1 signaling pathway. On the other hand, metformin can also inhibit mTOR directly and in an AMPK-independent manner. Thus, in the current study, we aimed to investigate the effects of metformin on the development of morphine and/or methadone-induced tolerance in human glioblastoma (T98G) cell line. We examined the effects of chronic treatment of morphine and/or methadone in the presence or absence of metformin with or without AMPK inhibitor (dorsomorphin hydrochloride) on levels of nitric oxide and cyclic adenosine monophosphate (cAMP), phosphorylated and dephosphorylated ribosomal protein S6 kinase β-1 (S6K1) and 4E-binding protein 1 (4E-BP1) in T98G cells. Pretreatment of cells with metformin (40 µM) with or without AMPK inhibitor (dorsomorphin hydrochloride; 1 µM) before adding of morphine (2.5 µM) or methadone (1 µM) revealed a protective effects on the development of opioid tolerance. Prior administration of metformin reversed the elevation of nitric oxide levels induced by morphine (p < 0.001) and methadone (p < 0.001) and also prevented the raise of cAMP levels induced by morphine in T98G cells (p < 0.05). Contribution of mTOR signaling pathway in metformin-induced effect was shown by the inhibition of phosphorylation of S6K1 and 4E-BP1, the downstream targets of mTOR. mTOR activation suppresses opioid-induced antinociception, and its activity has also been increased during opioid tolerance. 相似文献
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Hasan Yousefi-Manesh Samira Shirooie Alireza Partoazar Vahid Nikoui Mohammad Reza Abdollahzadeh Estakhri Azam Bakhtiarian 《Journal of cellular biochemistry》2019,120(7):11853-11858
It has been proposed carbon tetrachloride (CCl4) intoxication due to the production of free radicals and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) overload results hepatotoxicity. Phosphatidylserine (PS) has shown antioxidant activity in numerous studies. Therefore, this study was aimed to investigate the effects of PS liposomes treatment against the CCl4-induced hepatotoxicity in a rat model. Male Wistar rats were treated with PS (10 mg/kg, oral) or phosphatidylcholine liposomes (PC) (10 mg/kg, oral) for 3 days before CCl4 (2 ml/kg; ip once on the third day) injection. The serum level of ALT, AST, and ALP were measured. Also, antioxidant assays were performed. Administration of PS with CCl4 significantly inhibited alterations in the serum levels of AST, ALP (**P < 0.01), and ALT (***P < 0.001) compared with control group. Furthermore, measurement of malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels indicated that PS significantly reduced reactive oxygen species. The results of the present study showed the hepatoprotective effects of PS against CCl4-induced hepatotoxicity in rats. 相似文献
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