Volume 14, Issue 6 (November & December 2023)
BCN 2023, 14(6): 867-878 |
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Sarvin Jahanbani1 
, Mehdi Khaksari2 , Fatemeh Sadat Bitaraf3 , Majid Rahmati4 , Kobra Foroughi1 , Asghar Shayannia * 3
, Mehdi Khaksari2 , Fatemeh Sadat Bitaraf3 , Majid Rahmati4 , Kobra Foroughi1 , Asghar Shayannia * 3
1- Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
2- Addiction Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.
3- Department of Medical Biotechnology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
4- Cancer Prevention Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.
2- Addiction Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.
3- Department of Medical Biotechnology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran.
4- Cancer Prevention Research Center, Shahroud University of Medical Sciences, Shahroud, Iran.
Abstract:
Introduction: Diabetic neuropathy is a well-known complication of diabetes. Recently, hyperglycemia-induced toxicity has been confirmed to participates in multiple cellular pathways typical for neural deterioration. Nicotinamide phosphoribosyltransferase/pre-b cell colony-enhancing factor (Nampt/PBEF)/visfatin is a novel endogenous ligand that some studies have shown its neuroprotective effects on neurodegenerative disease. Therefore, we hypothesized that visfatin may prevent high glucose (HG)-induced neurotoxicity by inhibiting apoptosis, autophagy, and reactive oxygen species (ROS) responses properly.
Methods: 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) at 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 the PC12 diabetic neuropathy model, we examined ROS response, apoptosis, and autophagy using ROS detection kit, flow cytometry, and real-time PCR/Western blot, respectively.
Results: We determined that HG concentration significantly increased the ROS level and apoptosis of diabetic PC12 cells. However, visfatin treatment significantly decreased the ROS production (P<0.05) and apoptosis of diabetic PC12 cells (P<0.0001). Beclin-1 messenger ribonucleic acid (mRNA) level (P<0.05) and light chain 3 (Lc3)-II protein level (P<0.05) showed that the autophagy pathway is impaired by HG concentrations.
Conclusion: We concluded that visfatin can sufficiently decrease neural damage caused by ROS production and apoptosis under HG-induced toxicity.
Methods: 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) at 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 the PC12 diabetic neuropathy model, we examined ROS response, apoptosis, and autophagy using ROS detection kit, flow cytometry, and real-time PCR/Western blot, respectively.
Results: We determined that HG concentration significantly increased the ROS level and apoptosis of diabetic PC12 cells. However, visfatin treatment significantly decreased the ROS production (P<0.05) and apoptosis of diabetic PC12 cells (P<0.0001). Beclin-1 messenger ribonucleic acid (mRNA) level (P<0.05) and light chain 3 (Lc3)-II protein level (P<0.05) showed that the autophagy pathway is impaired by HG concentrations.
Conclusion: We concluded that visfatin can sufficiently decrease neural damage caused by ROS production and apoptosis under HG-induced toxicity.
Type of Study: Original |
Subject:
Cellular and molecular Neuroscience
Received: 2021/01/22 | Accepted: 2021/08/23 | Published: 2023/11/22
Received: 2021/01/22 | Accepted: 2021/08/23 | Published: 2023/11/22
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