Acacetin Prevents Renal Damage Induced by Streptozotocin via Altering the NF-κB/ASC/NLRP3 and AMPK/SIRT1 Pathways in Mice.

IF 3.2 4区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Qingfei Yu, Hongyan Mao, Annamalai Vijayalakshmi, Meilan Zhou
{"title":"Acacetin Prevents Renal Damage Induced by Streptozotocin via Altering the NF-κB/ASC/NLRP3 and AMPK/SIRT1 Pathways in Mice.","authors":"Qingfei Yu, Hongyan Mao, Annamalai Vijayalakshmi, Meilan Zhou","doi":"10.1002/bab.2753","DOIUrl":null,"url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is the most common cause of end-stage renal disease. Its pathogenesis includes inflammation, an excess of reactive oxygen species, and kidney damage. The present study intended to explore the nephroprotective effects of acacetin (ACN) in streptozotocin-induced diabetic animals. The following are the experimental groups: One millilitre of 0.9% saline was given to Group I (control), Streptozotocin (STZ) (diabetic animals) + 0.9% saline to Group II (DN group) (negative control), DN + ACN (15 mg/kg body weight [bw]) to Group III, and DN + Valsartan (150 mg/kg bw) to Group IV. According to the findings, ACN decreased the levels of glucose, serum creatinine (Scr), blood urea nitrogen (BUN), malondialdehyde (MDA), and proinflammatory cytokines while increasing the bw, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in comparison to the DN animals. The histopathological analysis revealed that the animals treated with ACN showed recovery of renal damage in the tissues caused by STZ. In the STZ-induced DN mice, ACN reduced renal damage by upregulating the proteins of 5' adenosine monophosphate-activated protein kinase (AMPK), p-AMPK, and SIRT1 and downregulating the proteins of TGF-β, COL-1, COL-IV, NF-κB, ASC, NLRP3, and GSDMD, according to western blot analysis. Hence, the current study demonstrated that the regulation of the AMPK/SIRT1 and NF-κB/ASC/NLRP3 inflammasome pathways in DN mice was responsible for the protective effects of ACN. ACN may therefore be a viable treatment option for DN.</p>","PeriodicalId":9274,"journal":{"name":"Biotechnology and applied biochemistry","volume":" ","pages":"e2753"},"PeriodicalIF":3.2000,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biotechnology and applied biochemistry","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1002/bab.2753","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease. Its pathogenesis includes inflammation, an excess of reactive oxygen species, and kidney damage. The present study intended to explore the nephroprotective effects of acacetin (ACN) in streptozotocin-induced diabetic animals. The following are the experimental groups: One millilitre of 0.9% saline was given to Group I (control), Streptozotocin (STZ) (diabetic animals) + 0.9% saline to Group II (DN group) (negative control), DN + ACN (15 mg/kg body weight [bw]) to Group III, and DN + Valsartan (150 mg/kg bw) to Group IV. According to the findings, ACN decreased the levels of glucose, serum creatinine (Scr), blood urea nitrogen (BUN), malondialdehyde (MDA), and proinflammatory cytokines while increasing the bw, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) in comparison to the DN animals. The histopathological analysis revealed that the animals treated with ACN showed recovery of renal damage in the tissues caused by STZ. In the STZ-induced DN mice, ACN reduced renal damage by upregulating the proteins of 5' adenosine monophosphate-activated protein kinase (AMPK), p-AMPK, and SIRT1 and downregulating the proteins of TGF-β, COL-1, COL-IV, NF-κB, ASC, NLRP3, and GSDMD, according to western blot analysis. Hence, the current study demonstrated that the regulation of the AMPK/SIRT1 and NF-κB/ASC/NLRP3 inflammasome pathways in DN mice was responsible for the protective effects of ACN. ACN may therefore be a viable treatment option for DN.

阿卡西汀通过改变小鼠的 NF-κB/ASC/NLRP3 和 AMPK/SIRT1 通路预防链脲佐菌素诱发的肾损伤
糖尿病肾病(DN)是终末期肾脏疾病最常见的病因。其发病机制包括炎症、活性氧过量和肾损害。本研究旨在探讨阿曲素(ACN)对链脲佐菌素诱导的糖尿病动物的肾保护作用。实验组如下:ⅰ组(对照组)给予1 ml 0.9%生理盐水,ⅱ组(DN组)给予1 ml链脲脲素(STZ) + 0.9%生理盐水(阴性对照组),ⅲ组给予DN + ACN (15 mg/kg体重[bw]),ⅳ组给予DN +缬沙坦(150 mg/kg体重[bw])。结果表明,ACN降低血糖、血清肌酐(Scr)、尿素氮(BUN)、丙二醛(MDA)、促炎细胞因子水平,升高体重、超氧化物歧化酶(SOD)、和谷胱甘肽过氧化物酶(GSH-Px)。组织病理学分析显示,经ACN处理后,STZ引起的肾组织损伤得以恢复。western blot分析显示,在stz诱导的DN小鼠中,ACN通过上调5′腺苷单磷酸活化蛋白激酶(AMPK)、p-AMPK和SIRT1蛋白,下调TGF-β、COL-1、COL-IV、NF-κB、ASC、NLRP3和GSDMD蛋白来减轻肾损伤。因此,本研究表明,ACN对DN小鼠炎症小体通路AMPK/SIRT1和NF-κB/ASC/NLRP3的调控是其保护作用的机制。因此ACN可能是DN的一种可行的治疗选择。
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 求助全文
来源期刊
Biotechnology and applied biochemistry
Biotechnology and applied biochemistry 工程技术-生化与分子生物学
CiteScore
6.00
自引率
7.10%
发文量
117
审稿时长
3 months
期刊介绍: Published since 1979, Biotechnology and Applied Biochemistry is dedicated to the rapid publication of high quality, significant research at the interface between life sciences and their technological exploitation. The Editors will consider papers for publication based on their novelty and impact as well as their contribution to the advancement of medical biotechnology and industrial biotechnology, covering cutting-edge research in synthetic biology, systems biology, metabolic engineering, bioengineering, biomaterials, biosensing, and nano-biotechnology.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信