{"title":"石斛碱通过调节自噬对心肌梗死大鼠心功能障碍的影响","authors":"Juan Fan, Yi Zhang","doi":"10.1166/jbt.2023.3227","DOIUrl":null,"url":null,"abstract":"Aim: To observe Dendrobine (Den) on rats with post-myocardial infarction cardiac dysfunction and mechanism. Materials: Dividing 27 rats as Sham, Model and Den groups, rats treated with two weeks of drug had their cardiac function and structure measured by ultrasound; their myocardial\n pathological changes observed by HE and Masson staining and observe apoptosis cell number by TUNEL staining; their serum activities of LDH and CK-MB detected by ELISA; myocardial autophagy protein expressions detected by WB and immunohistochemistry. Results: Model group displayed decreased\n cardiac function levels, enlarged area of myocardial fibrosis, more serum activities of LDH and CK-MB, increased myocardial tissue structural damage and apoptosis cell number, downregulated LAMP2 expression, and up-regulated expressions of Beclin1, LC3-II/LC3-I rate, and P62. To rat victims\n of myocardial infarction, Den improved cardiac function, reduced area of myocardial fibrosis, compromised activities of serum LDH and CK-MB, and relieved damage in myocardial structure, decreased apoptosis cell number in myocardial tissue, up-regulated the expressions of Beclin1, LAMP2 and\n LC3-II, and down-regulated P62 to promote the autophagy in myocardium damaged by myocardial infarction. Conclusion: Den alleviates post-myocardial infarction cardiac dysfunction through improvement of autophagosomes formation and autophagic flux via Beclin1/LAMP2 pathway.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effect of Dendrobine on Cardiac Dysfunction in Rats with Myocardial Infarction by Regulating Autophagy\",\"authors\":\"Juan Fan, Yi Zhang\",\"doi\":\"10.1166/jbt.2023.3227\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Aim: To observe Dendrobine (Den) on rats with post-myocardial infarction cardiac dysfunction and mechanism. Materials: Dividing 27 rats as Sham, Model and Den groups, rats treated with two weeks of drug had their cardiac function and structure measured by ultrasound; their myocardial\\n pathological changes observed by HE and Masson staining and observe apoptosis cell number by TUNEL staining; their serum activities of LDH and CK-MB detected by ELISA; myocardial autophagy protein expressions detected by WB and immunohistochemistry. Results: Model group displayed decreased\\n cardiac function levels, enlarged area of myocardial fibrosis, more serum activities of LDH and CK-MB, increased myocardial tissue structural damage and apoptosis cell number, downregulated LAMP2 expression, and up-regulated expressions of Beclin1, LC3-II/LC3-I rate, and P62. To rat victims\\n of myocardial infarction, Den improved cardiac function, reduced area of myocardial fibrosis, compromised activities of serum LDH and CK-MB, and relieved damage in myocardial structure, decreased apoptosis cell number in myocardial tissue, up-regulated the expressions of Beclin1, LAMP2 and\\n LC3-II, and down-regulated P62 to promote the autophagy in myocardium damaged by myocardial infarction. Conclusion: Den alleviates post-myocardial infarction cardiac dysfunction through improvement of autophagosomes formation and autophagic flux via Beclin1/LAMP2 pathway.\",\"PeriodicalId\":15300,\"journal\":{\"name\":\"Journal of Biomaterials and Tissue Engineering\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.1000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Biomaterials and Tissue Engineering\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1166/jbt.2023.3227\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.3227","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Effect of Dendrobine on Cardiac Dysfunction in Rats with Myocardial Infarction by Regulating Autophagy
Aim: To observe Dendrobine (Den) on rats with post-myocardial infarction cardiac dysfunction and mechanism. Materials: Dividing 27 rats as Sham, Model and Den groups, rats treated with two weeks of drug had their cardiac function and structure measured by ultrasound; their myocardial
pathological changes observed by HE and Masson staining and observe apoptosis cell number by TUNEL staining; their serum activities of LDH and CK-MB detected by ELISA; myocardial autophagy protein expressions detected by WB and immunohistochemistry. Results: Model group displayed decreased
cardiac function levels, enlarged area of myocardial fibrosis, more serum activities of LDH and CK-MB, increased myocardial tissue structural damage and apoptosis cell number, downregulated LAMP2 expression, and up-regulated expressions of Beclin1, LC3-II/LC3-I rate, and P62. To rat victims
of myocardial infarction, Den improved cardiac function, reduced area of myocardial fibrosis, compromised activities of serum LDH and CK-MB, and relieved damage in myocardial structure, decreased apoptosis cell number in myocardial tissue, up-regulated the expressions of Beclin1, LAMP2 and
LC3-II, and down-regulated P62 to promote the autophagy in myocardium damaged by myocardial infarction. Conclusion: Den alleviates post-myocardial infarction cardiac dysfunction through improvement of autophagosomes formation and autophagic flux via Beclin1/LAMP2 pathway.