Weibin Qin, Liyan Yu, Weizhi Tang, Meng Wang, Lin Lin, Qingwei Zhang, Feifei Yang, Guixin He
{"title":"芪参益气滴丸联合外泌体通过miRNA-155-5P调控巨噬细胞极化减轻心肌I/R损伤","authors":"Weibin Qin, Liyan Yu, Weizhi Tang, Meng Wang, Lin Lin, Qingwei Zhang, Feifei Yang, Guixin He","doi":"10.2174/011574888X408846251007045430","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>To investigate the protective mechanism of Qishen Yiqi Dropping Pills (Qishen) and its key active ingredients in combination with exosomes from bone marrow mesenchymal stem cells (BMSCs) against myocardial ischemia/reperfusion (I/R) injury.</p><p><strong>Methods: </strong>Infarct area was assessed by Evan's Blue/TTC double staining, myocardial apoptosis was analyzed by TUNEL staining, ATP content and NAD+/NADH ratio were detected biochemically, macrophage phenotype of myocardial tissues was detected by flow cytometry, activation of the mTOR/PI3K/Akt pathway was detected by Western blotting, and miR-155-5p expression was detected by qRT-PCR. 155-5p expression. Exo were given to identify the M1/M2 phenotypic transition by immunofluorescence, and the molecular mechanism was verified as in the in vivo experiments.</p><p><strong>Results: </strong>Compared with the model group, the Qishen, ginsenoside, and Exo group significantly reduced the infarcted area of the heart and promoted M2 and M2 phenotypic conversion, promoted M2- type macrophage infiltration, up-regulated the p-Akt/Akt ratio, and inhibited the expression of miR- 155-5p, but the combination therapy group did not show a synergistic effect, but the above protective effects were significantly weakened by the removal of macrophages. Ginsenoside and Exo synergistically promoted M2 polarization, activated the mTOR/PI3K/Akt pathway and upregulated miR-155-5p expression.</p><p><strong>Discussion: </strong>Qishen, particularly its active component ginsenoside, synergizes with BMSC-Exo to alleviate myocardial I/R injury by modulating macrophage polarization via the miR-155- 5p/mTOR/PI3K/Akt signaling axis.</p><p><strong>Conclusion: </strong>Qishen synergistically regulates the miR-155-5p/mTOR/PI3K/Akt signaling axis through ginsenoside components in BMSCs exosomes, promoting macrophage polarization toward M2-type, improving myocardial energy metabolism and attenuating I/R injury, and this protective effect is macrophage-dependent.</p>","PeriodicalId":93971,"journal":{"name":"Current stem cell research & therapy","volume":" ","pages":"316-331"},"PeriodicalIF":2.2000,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Qishen Yiqi Dropping Pills Combined with Exosomes Alleviate Myocardial I/R Injury by Regulating Macrophage Polarization <i>via miRNA-155-5P</i>.\",\"authors\":\"Weibin Qin, Liyan Yu, Weizhi Tang, Meng Wang, Lin Lin, Qingwei Zhang, Feifei Yang, Guixin He\",\"doi\":\"10.2174/011574888X408846251007045430\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>To investigate the protective mechanism of Qishen Yiqi Dropping Pills (Qishen) and its key active ingredients in combination with exosomes from bone marrow mesenchymal stem cells (BMSCs) against myocardial ischemia/reperfusion (I/R) injury.</p><p><strong>Methods: </strong>Infarct area was assessed by Evan's Blue/TTC double staining, myocardial apoptosis was analyzed by TUNEL staining, ATP content and NAD+/NADH ratio were detected biochemically, macrophage phenotype of myocardial tissues was detected by flow cytometry, activation of the mTOR/PI3K/Akt pathway was detected by Western blotting, and miR-155-5p expression was detected by qRT-PCR. 155-5p expression. Exo were given to identify the M1/M2 phenotypic transition by immunofluorescence, and the molecular mechanism was verified as in the in vivo experiments.</p><p><strong>Results: </strong>Compared with the model group, the Qishen, ginsenoside, and Exo group significantly reduced the infarcted area of the heart and promoted M2 and M2 phenotypic conversion, promoted M2- type macrophage infiltration, up-regulated the p-Akt/Akt ratio, and inhibited the expression of miR- 155-5p, but the combination therapy group did not show a synergistic effect, but the above protective effects were significantly weakened by the removal of macrophages. Ginsenoside and Exo synergistically promoted M2 polarization, activated the mTOR/PI3K/Akt pathway and upregulated miR-155-5p expression.</p><p><strong>Discussion: </strong>Qishen, particularly its active component ginsenoside, synergizes with BMSC-Exo to alleviate myocardial I/R injury by modulating macrophage polarization via the miR-155- 5p/mTOR/PI3K/Akt signaling axis.</p><p><strong>Conclusion: </strong>Qishen synergistically regulates the miR-155-5p/mTOR/PI3K/Akt signaling axis through ginsenoside components in BMSCs exosomes, promoting macrophage polarization toward M2-type, improving myocardial energy metabolism and attenuating I/R injury, and this protective effect is macrophage-dependent.</p>\",\"PeriodicalId\":93971,\"journal\":{\"name\":\"Current stem cell research & therapy\",\"volume\":\" \",\"pages\":\"316-331\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2026-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current stem cell research & therapy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/011574888X408846251007045430\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current stem cell research & therapy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/011574888X408846251007045430","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Qishen Yiqi Dropping Pills Combined with Exosomes Alleviate Myocardial I/R Injury by Regulating Macrophage Polarization via miRNA-155-5P.
Introduction: To investigate the protective mechanism of Qishen Yiqi Dropping Pills (Qishen) and its key active ingredients in combination with exosomes from bone marrow mesenchymal stem cells (BMSCs) against myocardial ischemia/reperfusion (I/R) injury.
Methods: Infarct area was assessed by Evan's Blue/TTC double staining, myocardial apoptosis was analyzed by TUNEL staining, ATP content and NAD+/NADH ratio were detected biochemically, macrophage phenotype of myocardial tissues was detected by flow cytometry, activation of the mTOR/PI3K/Akt pathway was detected by Western blotting, and miR-155-5p expression was detected by qRT-PCR. 155-5p expression. Exo were given to identify the M1/M2 phenotypic transition by immunofluorescence, and the molecular mechanism was verified as in the in vivo experiments.
Results: Compared with the model group, the Qishen, ginsenoside, and Exo group significantly reduced the infarcted area of the heart and promoted M2 and M2 phenotypic conversion, promoted M2- type macrophage infiltration, up-regulated the p-Akt/Akt ratio, and inhibited the expression of miR- 155-5p, but the combination therapy group did not show a synergistic effect, but the above protective effects were significantly weakened by the removal of macrophages. Ginsenoside and Exo synergistically promoted M2 polarization, activated the mTOR/PI3K/Akt pathway and upregulated miR-155-5p expression.
Discussion: Qishen, particularly its active component ginsenoside, synergizes with BMSC-Exo to alleviate myocardial I/R injury by modulating macrophage polarization via the miR-155- 5p/mTOR/PI3K/Akt signaling axis.
Conclusion: Qishen synergistically regulates the miR-155-5p/mTOR/PI3K/Akt signaling axis through ginsenoside components in BMSCs exosomes, promoting macrophage polarization toward M2-type, improving myocardial energy metabolism and attenuating I/R injury, and this protective effect is macrophage-dependent.
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