{"title":"烟酰胺磷酸核糖基转移酶/前 B 细胞集落增强因子/Visfatin 在糖尿病神经病变体外模型中预防高血糖诱导的神经毒性的有效性","authors":"Sarvin Jahanbani, Mehdi Khaksari, Fatemeh Sadat Bitaraf, Majid Rahmati, Kobra Foroughi, Asghar Shayannia","doi":"10.32598/bcn.2021.2870.2","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>We concluded that visfatin can sufficiently decrease neural damage caused by ROS production and apoptosis under HG-induced toxicity.</p><p><strong>Highlights: </strong>High glucose significantly increased the ROS level and apoptosis of diabetic PC12 cells;The autophagy pathway is impaired by high glucose;Nampt/PBEF/visfatin can significantly reduce neural damage caused by ROS production and apoptosis of diabetic PC12 cells.</p><p><strong>Plain language summary: </strong>Diabetes mellitus is a metabolic disorder characterized by hyperglycemia resulting from a failure in insulin secretion, insulin action, or both. Visfatin (Nampt/PBEF) has insulin-mimetic effects. So far, no study has assessed its effects on diabetic neuropathy. Therefore, we examined the neuroprotective effects of visfatin on cell line 12 (PC12) against glucose-induced neurotoxicity. Based on the results, it was concluded that the Nampt/PBEF/visfatin can significantly reduce neural damage caused by production of reactive oxygen species and apoptosis of diabetic PC12 cell.</p>","PeriodicalId":20362,"journal":{"name":"Polar Biology","volume":"36 1","pages":"867-878"},"PeriodicalIF":1.5000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11273206/pdf/","citationCount":"0","resultStr":"{\"title\":\"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.\",\"authors\":\"Sarvin Jahanbani, Mehdi Khaksari, Fatemeh Sadat Bitaraf, Majid Rahmati, Kobra Foroughi, Asghar Shayannia\",\"doi\":\"10.32598/bcn.2021.2870.2\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>We concluded that visfatin can sufficiently decrease neural damage caused by ROS production and apoptosis under HG-induced toxicity.</p><p><strong>Highlights: </strong>High glucose significantly increased the ROS level and apoptosis of diabetic PC12 cells;The autophagy pathway is impaired by high glucose;Nampt/PBEF/visfatin can significantly reduce neural damage caused by ROS production and apoptosis of diabetic PC12 cells.</p><p><strong>Plain language summary: </strong>Diabetes mellitus is a metabolic disorder characterized by hyperglycemia resulting from a failure in insulin secretion, insulin action, or both. Visfatin (Nampt/PBEF) has insulin-mimetic effects. So far, no study has assessed its effects on diabetic neuropathy. Therefore, we examined the neuroprotective effects of visfatin on cell line 12 (PC12) against glucose-induced neurotoxicity. Based on the results, it was concluded that the Nampt/PBEF/visfatin can significantly reduce neural damage caused by production of reactive oxygen species and apoptosis of diabetic PC12 cell.</p>\",\"PeriodicalId\":20362,\"journal\":{\"name\":\"Polar Biology\",\"volume\":\"36 1\",\"pages\":\"867-878\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2023-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11273206/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Polar Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.32598/bcn.2021.2870.2\",\"RegionNum\":4,\"RegionCategory\":\"环境科学与生态学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIODIVERSITY CONSERVATION\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Polar Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.32598/bcn.2021.2870.2","RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIODIVERSITY CONSERVATION","Score":null,"Total":0}
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.
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.
Highlights: High glucose significantly increased the ROS level and apoptosis of diabetic PC12 cells;The autophagy pathway is impaired by high glucose;Nampt/PBEF/visfatin can significantly reduce neural damage caused by ROS production and apoptosis of diabetic PC12 cells.
Plain language summary: Diabetes mellitus is a metabolic disorder characterized by hyperglycemia resulting from a failure in insulin secretion, insulin action, or both. Visfatin (Nampt/PBEF) has insulin-mimetic effects. So far, no study has assessed its effects on diabetic neuropathy. Therefore, we examined the neuroprotective effects of visfatin on cell line 12 (PC12) against glucose-induced neurotoxicity. Based on the results, it was concluded that the Nampt/PBEF/visfatin can significantly reduce neural damage caused by production of reactive oxygen species and apoptosis of diabetic PC12 cell.
期刊介绍:
Polar Biology publishes Original Papers, Reviews, and Short Notes and is the focal point for biologists working in polar regions. It is also of interest to scientists working in biology in general, ecology and physiology, as well as in oceanography and climatology related to polar life. Polar Biology presents results of studies in plants, animals, and micro-organisms of marine, limnic and terrestrial habitats in polar and subpolar regions of both hemispheres.
Taxonomy/ Biogeography
Life History
Spatio-temporal Patterns in Abundance and Diversity
Ecological Interactions
Trophic Ecology
Ecophysiology/ Biochemistry of Adaptation
Biogeochemical Pathways and Cycles
Ecological Models
Human Impact/ Climate Change/ Conservation