Rui Sun, Wei-Yi Huang, Zi-Yang Guo, Fang Liu, Qiang Sun, Wen-Jun Fan, Dan-Mei Huang, Yan-Mei Zhang, Fen-Fei Gao, Bin Wang
{"title":"三七皂苷R1通过激活Wnt/β-Catenin信号抑制细胞凋亡改善心肌缺血/再灌注损伤","authors":"Rui Sun, Wei-Yi Huang, Zi-Yang Guo, Fang Liu, Qiang Sun, Wen-Jun Fan, Dan-Mei Huang, Yan-Mei Zhang, Fen-Fei Gao, Bin Wang","doi":"10.1142/S0192415X2550082X","DOIUrl":null,"url":null,"abstract":"<p><p>Notoginsenoside R1 (NGR1), a natural triterpenoid saponin, is extracted from <i>Panax notoginseng</i>, and has cardiovascular and cerebrovascular protective effects due to anti-inflammatory, anti-oxidant, and anti-apoptotic properties. Previous research has suggested a protective role for NGR1 in myocardial ischemia/reperfusion (MI/R) injury. However, the potential mechanisms involved have not been fully elucidated. Thus, the objective of our study was to validate the protective role of NGR1 in MI/R injury and to investigate its underlying mechanisms. Results showed that, in mice, NGR1 substantially improved heart function, reduced infarct area, and inhibited cardiomyocyte apoptosis. Mechanistically, network pharmacological predictions suggested that NGR1 could inhibit apoptosis by activating the Wnt signaling pathway. Experimentally, the protective effects of NGR1 in inhibiting cardiomyocyte apoptosis, improving cardiac function, and reducing infarct size were significantly attenuated with the use of the Wnt signaling inhibitor XAV-939. Collectively, our investigation demonstrated that NGR1 improves myocardial injury triggered by ischemia/reperfusion (I/R) by enhancing Wnt/[Formula: see text]-catenin pathway activity, which in turn suppresses apoptosis.</p>","PeriodicalId":94221,"journal":{"name":"The American journal of Chinese medicine","volume":" ","pages":"2223-2243"},"PeriodicalIF":5.5000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Notoginsenoside R1 Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Apoptosis via Activating Wnt/β-Catenin Signaling.\",\"authors\":\"Rui Sun, Wei-Yi Huang, Zi-Yang Guo, Fang Liu, Qiang Sun, Wen-Jun Fan, Dan-Mei Huang, Yan-Mei Zhang, Fen-Fei Gao, Bin Wang\",\"doi\":\"10.1142/S0192415X2550082X\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Notoginsenoside R1 (NGR1), a natural triterpenoid saponin, is extracted from <i>Panax notoginseng</i>, and has cardiovascular and cerebrovascular protective effects due to anti-inflammatory, anti-oxidant, and anti-apoptotic properties. Previous research has suggested a protective role for NGR1 in myocardial ischemia/reperfusion (MI/R) injury. However, the potential mechanisms involved have not been fully elucidated. Thus, the objective of our study was to validate the protective role of NGR1 in MI/R injury and to investigate its underlying mechanisms. Results showed that, in mice, NGR1 substantially improved heart function, reduced infarct area, and inhibited cardiomyocyte apoptosis. Mechanistically, network pharmacological predictions suggested that NGR1 could inhibit apoptosis by activating the Wnt signaling pathway. Experimentally, the protective effects of NGR1 in inhibiting cardiomyocyte apoptosis, improving cardiac function, and reducing infarct size were significantly attenuated with the use of the Wnt signaling inhibitor XAV-939. Collectively, our investigation demonstrated that NGR1 improves myocardial injury triggered by ischemia/reperfusion (I/R) by enhancing Wnt/[Formula: see text]-catenin pathway activity, which in turn suppresses apoptosis.</p>\",\"PeriodicalId\":94221,\"journal\":{\"name\":\"The American journal of Chinese medicine\",\"volume\":\" \",\"pages\":\"2223-2243\"},\"PeriodicalIF\":5.5000,\"publicationDate\":\"2025-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The American journal of Chinese medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1142/S0192415X2550082X\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/9/10 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The American journal of Chinese medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1142/S0192415X2550082X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/9/10 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
Notoginsenoside R1 Ameliorates Myocardial Ischemia/Reperfusion Injury by Suppressing Apoptosis via Activating Wnt/β-Catenin Signaling.
Notoginsenoside R1 (NGR1), a natural triterpenoid saponin, is extracted from Panax notoginseng, and has cardiovascular and cerebrovascular protective effects due to anti-inflammatory, anti-oxidant, and anti-apoptotic properties. Previous research has suggested a protective role for NGR1 in myocardial ischemia/reperfusion (MI/R) injury. However, the potential mechanisms involved have not been fully elucidated. Thus, the objective of our study was to validate the protective role of NGR1 in MI/R injury and to investigate its underlying mechanisms. Results showed that, in mice, NGR1 substantially improved heart function, reduced infarct area, and inhibited cardiomyocyte apoptosis. Mechanistically, network pharmacological predictions suggested that NGR1 could inhibit apoptosis by activating the Wnt signaling pathway. Experimentally, the protective effects of NGR1 in inhibiting cardiomyocyte apoptosis, improving cardiac function, and reducing infarct size were significantly attenuated with the use of the Wnt signaling inhibitor XAV-939. Collectively, our investigation demonstrated that NGR1 improves myocardial injury triggered by ischemia/reperfusion (I/R) by enhancing Wnt/[Formula: see text]-catenin pathway activity, which in turn suppresses apoptosis.