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Basic and Clinical Neuroscience، جلد ۱۴، شماره ۶، صفحات ۰-۰
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| عنوان فارسی |
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| چکیده فارسی مقاله |
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| عنوان انگلیسی |
Nampt/PBEF/Visfatin Protects PC12 against High Glucose-Induced Neurotoxicity in an in vitro Model of Diabetic Neuropathy via Inhibiting Oxidative Stress, Autophagy and Apoptosis |
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| چکیده انگلیسی مقاله |
Diabetic neuropathy is a well-known complication of diabetes. It has been recently confirmed that hyperglycemia-induced toxicity participates in multiple cellular pathways that are typical for neural deterioration. Nampt/PBEF/visfatin is a novel endogenous ligand, which some studies have shown its neuroprotective effects on neurodegenerative disease. Therefore, we hypothesized that visfatin might prevent high glucose (HG)-induced neurotoxicity via the inhibition of apoptosis, autophagy, and reactive oxygen species (ROS) responses properly. In this study, Pheochromocytoma Cell Line 12 (PC12) cells were exposed to both HG concentrations (50, 75, 100,125, 150 mM) and visfatin (50, 100, 150 ng/ml) in different time-points to determine the optimum time and dose of glucose and visfatin. To investigate the effects of visfatin on HG-induced damage in PC12 diabetic neuropathy model, we examined ROS response, apoptosis, and autophagy by using ROS detection kit, flow cytometry, and Real-time PCR/western blot, respectively. We determined that HG concentration significantly increased ROS level and apoptosis of diabetic PC12 cells. However, visfatin treatment significantly decreased ROS production (P < 0.05) and apoptosis of diabetic PC12 cells (P < 0.0001). Beclin-1 mRNA level (P < 0.05) and Lc3-II protein level (P < 0.05) showed that autophagy pathway is impaired by HG concentrations. We concluded that visfatin could sufficiently decrease neural damage caused by ROS production and apoptosis under HG-induced toxicity. |
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| کلیدواژه‌های انگلیسی مقاله |
Visfatin, Diabetic Neuropathy, Antioxidant, Apoptosis, Autophagy |
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| نویسندگان مقاله |
| Sarvin Jahanbani
Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
| Mehdi khaksari
Addiction Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.
| Fatemeh Sadat Bitaraf
Department of Medical Biotechnology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
| Majid Rahmati
Cancer Prevention Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.
| Kobra Foroughi
Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
| Asghar Shayannia
Department of Medical Biotechnology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
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| نشانی اینترنتی |
http://bcn.iums.ac.ir/browse.php?a_code=A-10-2870-2&slc_lang=en&sid=1 |
| فایل مقاله |
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| کد مقاله (doi) |
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| زبان مقاله منتشر شده |
en |
| موضوعات مقاله منتشر شده |
Cellular and molecular Neuroscience |
| نوع مقاله منتشر شده |
Original |
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