دوره 14، شماره 6 - ( 8-1402 )
جلد 14 شماره 6 صفحات 878-867 |
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Jahanbani S, khaksari M, Bitaraf F S, Rahmati M, Foroughi K, Shayannia A. Effectiveness of Nicotinamide Phosphoribosyltransferase/Pre-B Cell Colony-enhancing Factor/ Visfatin in preventing High Glucose-induced Neurotoxicity in an In-vitro Model of Diabetic Neuropathy. BCN 2023; 14 (6) :867-878
URL: http://bcn.iums.ac.ir/article-1-2071-fa.html
URL: http://bcn.iums.ac.ir/article-1-2071-fa.html
Effectiveness of Nicotinamide Phosphoribosyltransferase/Pre-B Cell Colony-enhancing Factor/ Visfatin in preventing High Glucose-induced Neurotoxicity in an In-vitro Model of Diabetic Neuropathy. مجله علوم اعصاب پایه و بالینی. 1402; 14 (6) :867-878
چکیده:
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.
نوع مطالعه: Original |
موضوع مقاله:
Cellular and molecular Neuroscience
دریافت: 1399/11/3 | پذیرش: 1400/6/1 | انتشار: 1402/9/1
دریافت: 1399/11/3 | پذیرش: 1400/6/1 | انتشار: 1402/9/1
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