{"title":"清心解郁颗粒通过调节MK2/TTP通路减轻心肌梗死诱导的炎症反应。","authors":"Jianghan Qi, Xiaoyao Gao, Ying Han, Meiling Yang, Chenyi Wei, Ling Zhang, Jianfeng Chu","doi":"10.1080/13880209.2025.2467377","DOIUrl":null,"url":null,"abstract":"<p><strong>Context: </strong>Qing-Xin-Jie-Yu Granule (QXJYG) has shown promise in the treatment of myocardial infarction. However, the mechanism of action of QXJYG underlying its anti-inflammation remain unknown.</p><p><strong>Objective: </strong>The study aimed to evaluate the effectiveness and mechanism of QXJYG in a mouse model of myocardial infarction and hypoxia-induced H9C2 cells.</p><p><strong>Materials and methods: </strong>Myocardial infarction was induced in mice <i>via</i> left anterior descending coronary artery ligation, and hypoxia-induced H9C2 cells was served as the <i>in vitro</i> model. The cardiac function was evaluated by echocardiography, while myocardial tissue pathology was examined using HE and Masson's trichrome staining. Changes in serum markers of cardiac injury were measured using ELISA kits. The levels of inflammatory cytokines in both the serum and cardiac tissue were quantified using the Bio-Plex Pro Mouse Chemokine assay, and hypoxia-induced inflammatory factors in H9C2 cells were assessed by RT-qPCR. Additionally, western blot analysis was conducted to evaluate the expression of proteins related to the MK2/TTP signaling pathway both <i>in vivo</i> and <i>in vitro</i> experiments.</p><p><strong>Results: </strong>QXJYG significantly enhanced cardiac function in mice with myocardial infarction, as evidenced by improved myocardial tissue structure, reduced collagen fiber deposition, and lowered serum levels of creatine kinase isoenzyme MB (CK-MB), cardiac Troponin T (cTnT), and brain Natriuretic Peptide (BNP). QXJYG may reduce the expression of inflammatory factors in both the heart and serum of myocardial infarction-induced mice and attenuate hypoxia-induced levels of inflammatory factors in cardiomyocytes by decreasing the ratio of p-MK2/MK2 and increasing the protein expression of TTP.</p><p><strong>Discussion and conclusions: </strong>QXJYG improved cardiac function and reduced injury, fibrosis, and inflammation after myocardial infarction, likely through modulation of the MK2/TTP signaling pathway.</p>","PeriodicalId":19942,"journal":{"name":"Pharmaceutical Biology","volume":"63 1","pages":"128-140"},"PeriodicalIF":3.9000,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849043/pdf/","citationCount":"0","resultStr":"{\"title\":\"Qing-Xin-Jie-Yu Granule attenuates myocardial infarction-induced inflammatory response by regulating the MK2/TTP pathway.\",\"authors\":\"Jianghan Qi, Xiaoyao Gao, Ying Han, Meiling Yang, Chenyi Wei, Ling Zhang, Jianfeng Chu\",\"doi\":\"10.1080/13880209.2025.2467377\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Context: </strong>Qing-Xin-Jie-Yu Granule (QXJYG) has shown promise in the treatment of myocardial infarction. However, the mechanism of action of QXJYG underlying its anti-inflammation remain unknown.</p><p><strong>Objective: </strong>The study aimed to evaluate the effectiveness and mechanism of QXJYG in a mouse model of myocardial infarction and hypoxia-induced H9C2 cells.</p><p><strong>Materials and methods: </strong>Myocardial infarction was induced in mice <i>via</i> left anterior descending coronary artery ligation, and hypoxia-induced H9C2 cells was served as the <i>in vitro</i> model. The cardiac function was evaluated by echocardiography, while myocardial tissue pathology was examined using HE and Masson's trichrome staining. Changes in serum markers of cardiac injury were measured using ELISA kits. The levels of inflammatory cytokines in both the serum and cardiac tissue were quantified using the Bio-Plex Pro Mouse Chemokine assay, and hypoxia-induced inflammatory factors in H9C2 cells were assessed by RT-qPCR. Additionally, western blot analysis was conducted to evaluate the expression of proteins related to the MK2/TTP signaling pathway both <i>in vivo</i> and <i>in vitro</i> experiments.</p><p><strong>Results: </strong>QXJYG significantly enhanced cardiac function in mice with myocardial infarction, as evidenced by improved myocardial tissue structure, reduced collagen fiber deposition, and lowered serum levels of creatine kinase isoenzyme MB (CK-MB), cardiac Troponin T (cTnT), and brain Natriuretic Peptide (BNP). QXJYG may reduce the expression of inflammatory factors in both the heart and serum of myocardial infarction-induced mice and attenuate hypoxia-induced levels of inflammatory factors in cardiomyocytes by decreasing the ratio of p-MK2/MK2 and increasing the protein expression of TTP.</p><p><strong>Discussion and conclusions: </strong>QXJYG improved cardiac function and reduced injury, fibrosis, and inflammation after myocardial infarction, likely through modulation of the MK2/TTP signaling pathway.</p>\",\"PeriodicalId\":19942,\"journal\":{\"name\":\"Pharmaceutical Biology\",\"volume\":\"63 1\",\"pages\":\"128-140\"},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2025-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11849043/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pharmaceutical Biology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/13880209.2025.2467377\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/2/21 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MEDICAL LABORATORY TECHNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pharmaceutical Biology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13880209.2025.2467377","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/2/21 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
背景：清心解郁颗粒（QXJYG）在治疗心肌梗死方面显示出良好的前景。然而，芪xjyg的抗炎作用机制尚不清楚。目的：探讨清心健气对小鼠心肌梗死及缺氧诱导的H9C2细胞模型的作用及机制。材料与方法：采用左冠状动脉前降支结扎法诱导小鼠心肌梗死，以缺氧诱导的H9C2细胞为体外模型。超声心动图评价心脏功能，HE及马氏三色染色检查心肌组织病理。采用ELISA试剂盒检测心肌损伤血清标志物的变化。采用Bio-Plex Pro Mouse Chemokine assay定量血清和心脏组织中炎症因子的水平，采用RT-qPCR评估H9C2细胞中缺氧诱导的炎症因子。此外，在体内和体外实验中，通过western blot分析MK2/TTP信号通路相关蛋白的表达情况。结果：清肾益汤对心肌梗死小鼠心功能有明显改善，表现为心肌组织结构改善，胶原纤维沉积减少，血清肌酸激酶同功酶MB （CK-MB）、心肌肌钙蛋白T （cTnT）、脑钠肽（BNP）水平降低。QXJYG可能通过降低p-MK2/MK2比值和提高TTP蛋白表达，降低心肌梗死小鼠心脏和血清中炎症因子的表达，减弱缺氧诱导的心肌细胞中炎症因子的水平。讨论与结论：QXJYG改善心功能，减轻心肌梗死后的损伤、纤维化和炎症，可能通过调节MK2/TTP信号通路。
Qing-Xin-Jie-Yu Granule attenuates myocardial infarction-induced inflammatory response by regulating the MK2/TTP pathway.
Context: Qing-Xin-Jie-Yu Granule (QXJYG) has shown promise in the treatment of myocardial infarction. However, the mechanism of action of QXJYG underlying its anti-inflammation remain unknown.
Objective: The study aimed to evaluate the effectiveness and mechanism of QXJYG in a mouse model of myocardial infarction and hypoxia-induced H9C2 cells.
Materials and methods: Myocardial infarction was induced in mice via left anterior descending coronary artery ligation, and hypoxia-induced H9C2 cells was served as the in vitro model. The cardiac function was evaluated by echocardiography, while myocardial tissue pathology was examined using HE and Masson's trichrome staining. Changes in serum markers of cardiac injury were measured using ELISA kits. The levels of inflammatory cytokines in both the serum and cardiac tissue were quantified using the Bio-Plex Pro Mouse Chemokine assay, and hypoxia-induced inflammatory factors in H9C2 cells were assessed by RT-qPCR. Additionally, western blot analysis was conducted to evaluate the expression of proteins related to the MK2/TTP signaling pathway both in vivo and in vitro experiments.
Results: QXJYG significantly enhanced cardiac function in mice with myocardial infarction, as evidenced by improved myocardial tissue structure, reduced collagen fiber deposition, and lowered serum levels of creatine kinase isoenzyme MB (CK-MB), cardiac Troponin T (cTnT), and brain Natriuretic Peptide (BNP). QXJYG may reduce the expression of inflammatory factors in both the heart and serum of myocardial infarction-induced mice and attenuate hypoxia-induced levels of inflammatory factors in cardiomyocytes by decreasing the ratio of p-MK2/MK2 and increasing the protein expression of TTP.
Discussion and conclusions: QXJYG improved cardiac function and reduced injury, fibrosis, and inflammation after myocardial infarction, likely through modulation of the MK2/TTP signaling pathway.
期刊介绍：
Pharmaceutical Biology will publish manuscripts describing the discovery, methods for discovery, description, analysis characterization, and production/isolation (including sources and surveys) of biologically-active chemicals or other substances, drugs, pharmaceutical products, or preparations utilized in systems of traditional medicine.
Topics may generally encompass any facet of natural product research related to pharmaceutical biology. Papers dealing with agents or topics related to natural product drugs are also appropriate (e.g., semi-synthetic derivatives). Manuscripts will be published as reviews, perspectives, regular research articles, and short communications. The primary criteria for acceptance and publication are scientific rigor and potential to advance the field.
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