Activation of SIRT1 by silibinin improved mitochondrial health and alleviated the oxidative damage in experimental diabetic neuropathy and high glucose-mediated neurotoxicity.

IF 4.7 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-08-01 Epub Date: 2022-08-09 DOI:10.1080/13813455.2022.2108454

Islauddin Khan, Kumari Preeti, Rahul Kumar, Dharmendra Kumar Khatri, Shashi Bala Singh

{"title":"Activation of SIRT1 by silibinin improved mitochondrial health and alleviated the oxidative damage in experimental diabetic neuropathy and high glucose-mediated neurotoxicity.","authors":"Islauddin Khan, Kumari Preeti, Rahul Kumar, Dharmendra Kumar Khatri, Shashi Bala Singh","doi":"10.1080/13813455.2022.2108454","DOIUrl":null,"url":null,"abstract":"Background: Silibinin (SBN), a sirtuin 1 (SIRT1) activator, has been evaluated for its anti-inflammatory activity in many inflammatory diseases. However, its role in diabetes-induced peripheral neuropathy (DPN) remains unknown. The SIRT1 activation convalesces nerve functions by improving mitochondrial biogenesis and mitophagy.Methods: DPN was induced by streptozotocin (STZ) at a dose of 55 mg/kg, i.p. in the male SD rats whereas neurotoxicity was induced in Neuro2A cells by 30 mM (high glucose) glucose. Neurobehavioural (nerve conduction velocity and nerve blood flow) western blot, immunohistochemistry, and immunocytochemistry were performed to evaluate the protein expression and their cellular localisation.Results: Two-week SBN treatment improved neurobehavioural symptoms, SIRT1, PGC-1α, and TFAM expression in the sciatic nerve and HG insulted N2A cells. It has also maintained the mitophagy by up-regulating PARL, PINK1, PGAM5, LC3 level and provided antioxidant defence by upregulating Nrf2.Conclusion: SBN has shown neuroprotective potential in DPN through SIRT1 activation and antioxidant mechanism.","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":" ","pages":"420-436"},"PeriodicalIF":4.7000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13813455.2022.2108454","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/8/9 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Silibinin (SBN), a sirtuin 1 (SIRT1) activator, has been evaluated for its anti-inflammatory activity in many inflammatory diseases. However, its role in diabetes-induced peripheral neuropathy (DPN) remains unknown. The SIRT1 activation convalesces nerve functions by improving mitochondrial biogenesis and mitophagy.

Methods: DPN was induced by streptozotocin (STZ) at a dose of 55 mg/kg, i.p. in the male SD rats whereas neurotoxicity was induced in Neuro2A cells by 30 mM (high glucose) glucose. Neurobehavioural (nerve conduction velocity and nerve blood flow) western blot, immunohistochemistry, and immunocytochemistry were performed to evaluate the protein expression and their cellular localisation.

Results: Two-week SBN treatment improved neurobehavioural symptoms, SIRT1, PGC-1α, and TFAM expression in the sciatic nerve and HG insulted N2A cells. It has also maintained the mitophagy by up-regulating PARL, PINK1, PGAM5, LC3 level and provided antioxidant defence by upregulating Nrf2.

Conclusion: SBN has shown neuroprotective potential in DPN through SIRT1 activation and antioxidant mechanism.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

在实验性糖尿病神经病变和高糖介导的神经毒性中，西利宾激活 SIRT1 可改善线粒体健康，减轻氧化损伤。

背景：Silibinin (SBN)是一种sirtuin 1 (SIRT1)激活剂，其抗炎活性已在许多炎症性疾病中得到评估。然而，它在糖尿病诱发的周围神经病变（DPN）中的作用仍然未知。激活 SIRT1 可通过改善线粒体的生物生成和有丝分裂来恢复神经功能：方法：用 55 毫克/千克剂量的链脲佐菌素（STZ）诱导雄性 SD 大鼠发生 DPN，用 30 毫摩尔（高糖）葡萄糖诱导 Neuro2A 细胞发生神经毒性。对神经行为（神经传导速度和神经血流量）进行了免疫印迹、免疫组织化学和免疫细胞化学分析，以评估蛋白质的表达及其在细胞中的定位：结果：为期两周的 SBN 治疗改善了神经行为症状、SIRT1、PGC-1α 和 TFAM 在坐骨神经和受 HG 损伤的 N2A 细胞中的表达。它还能通过上调 PARL、PINK1、PGAM5 和 LC3 水平维持有丝分裂，并通过上调 Nrf2 提供抗氧化防御：结论：通过激活 SIRT1 和抗氧化机制，SBN 对 DPN 具有神经保护潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464

期刊介绍： ACS Applied Bio Materials is an interdisciplinary journal publishing original research covering all aspects of biomaterials and biointerfaces including and beyond the traditional biosensing, biomedical and therapeutic applications. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrates knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important bio applications. The journal is specifically interested in work that addresses the relationship between structure and function and assesses the stability and degradation of materials under relevant environmental and biological conditions.