Xingchen Wang, Lin Zhang, Runkun Wang, Wenfeng Hu, Jialin Sun, Lei Wang
{"title":"三七皂苷通过TLR4/NF-κB信号通路改善肾功能衰竭大鼠肾间质纤维化","authors":"Xingchen Wang, Lin Zhang, Runkun Wang, Wenfeng Hu, Jialin Sun, Lei Wang","doi":"10.1166/mex.2023.2546","DOIUrl":null,"url":null,"abstract":"Panax notoginseng saponins (PNS) have excellent effects on treating cardiovascular and cerebrovascular diseases, tumors and organ interstitial diseases. This study assessed the effect of PNS on renal interstitial fibrosis (RIF). Four groups of models were firstly created, which included; renal failure model, healthy group, model group, PNS group, and then established TLR4 inhibitor group (TAK-242 group), TLR4 activator group (LPS group), combined PNS and TLR4 inhibitor group (PNS+ TAK-242 group) and combined PNS and TLR4 agonist (PNS+LPS group). TLR4/NF- κ B signaling pathway and regulatory mechanism for PNS were observed along with analysis of TGF- β 1, α -SMA, Collagen I and FN expressions in kidney tissues. The PNS significantly inhibited changes of renal interstitial fibrosis in rats with renal failure, and this process was related to decreased expressions of TLR4 and NF- κ B. The PNS also inhibited the expression of TLR4, and expressions of TGF- β 1, α -SMA, Collagen I and FN were down-regulated in kidney cells after using TAK-242, especially in the PNS+TAK-242 group. The PNS can thus significantly inhibit the process of renal fibrosis, and this process is due to the fact that, PNS inhibits the activity of TLR4/NF- κ B signaling pathway to down-regulate the expressions of fibrosis-related factors TGF- β 1, α -SMA, etc., in exerting its effects.","PeriodicalId":18318,"journal":{"name":"Materials Express","volume":"105 3","pages":"0"},"PeriodicalIF":0.7000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Improvement on renal interstitial fibrosis in rats with renal failure via TLR4/NF-<i>κ</i>B signaling pathway by means of panax notoginseng saponins\",\"authors\":\"Xingchen Wang, Lin Zhang, Runkun Wang, Wenfeng Hu, Jialin Sun, Lei Wang\",\"doi\":\"10.1166/mex.2023.2546\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Panax notoginseng saponins (PNS) have excellent effects on treating cardiovascular and cerebrovascular diseases, tumors and organ interstitial diseases. This study assessed the effect of PNS on renal interstitial fibrosis (RIF). Four groups of models were firstly created, which included; renal failure model, healthy group, model group, PNS group, and then established TLR4 inhibitor group (TAK-242 group), TLR4 activator group (LPS group), combined PNS and TLR4 inhibitor group (PNS+ TAK-242 group) and combined PNS and TLR4 agonist (PNS+LPS group). TLR4/NF- κ B signaling pathway and regulatory mechanism for PNS were observed along with analysis of TGF- β 1, α -SMA, Collagen I and FN expressions in kidney tissues. The PNS significantly inhibited changes of renal interstitial fibrosis in rats with renal failure, and this process was related to decreased expressions of TLR4 and NF- κ B. The PNS also inhibited the expression of TLR4, and expressions of TGF- β 1, α -SMA, Collagen I and FN were down-regulated in kidney cells after using TAK-242, especially in the PNS+TAK-242 group. The PNS can thus significantly inhibit the process of renal fibrosis, and this process is due to the fact that, PNS inhibits the activity of TLR4/NF- κ B signaling pathway to down-regulate the expressions of fibrosis-related factors TGF- β 1, α -SMA, etc., in exerting its effects.\",\"PeriodicalId\":18318,\"journal\":{\"name\":\"Materials Express\",\"volume\":\"105 3\",\"pages\":\"0\"},\"PeriodicalIF\":0.7000,\"publicationDate\":\"2023-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Materials Express\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1166/mex.2023.2546\",\"RegionNum\":4,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Materials Science\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Materials Express","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1166/mex.2023.2546","RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Materials Science","Score":null,"Total":0}
Improvement on renal interstitial fibrosis in rats with renal failure via TLR4/NF-κB signaling pathway by means of panax notoginseng saponins
Panax notoginseng saponins (PNS) have excellent effects on treating cardiovascular and cerebrovascular diseases, tumors and organ interstitial diseases. This study assessed the effect of PNS on renal interstitial fibrosis (RIF). Four groups of models were firstly created, which included; renal failure model, healthy group, model group, PNS group, and then established TLR4 inhibitor group (TAK-242 group), TLR4 activator group (LPS group), combined PNS and TLR4 inhibitor group (PNS+ TAK-242 group) and combined PNS and TLR4 agonist (PNS+LPS group). TLR4/NF- κ B signaling pathway and regulatory mechanism for PNS were observed along with analysis of TGF- β 1, α -SMA, Collagen I and FN expressions in kidney tissues. The PNS significantly inhibited changes of renal interstitial fibrosis in rats with renal failure, and this process was related to decreased expressions of TLR4 and NF- κ B. The PNS also inhibited the expression of TLR4, and expressions of TGF- β 1, α -SMA, Collagen I and FN were down-regulated in kidney cells after using TAK-242, especially in the PNS+TAK-242 group. The PNS can thus significantly inhibit the process of renal fibrosis, and this process is due to the fact that, PNS inhibits the activity of TLR4/NF- κ B signaling pathway to down-regulate the expressions of fibrosis-related factors TGF- β 1, α -SMA, etc., in exerting its effects.