{"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.
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.