Protective effect of Guanxin Danshen formula on myocardial ischemia-reperfusion injury in rats

被引:1
|
作者
Li, Lanfang [1 ]
Liu, Bo [1 ]
Wang, Min [1 ]
Ye, Jingxue [1 ]
Sun, Guibo [1 ]
机构
[1] Peking Union Med Coll & Chinese Acad Med Sci, Inst Med Plant Dev, Beijing, Peoples R China
关键词
Myocardial Ischemia; Reperfusion; NLR Family; Pyrin Domain-Containing 3 Protein; Ginsenosides; INFARCTION; BIOLOGY;
D O I
10.1590/acb380123
中图分类号
R61 [外科手术学];
学科分类号
摘要
Purpose: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats. Methods: MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model. Results: The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1 beta, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1 beta, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor alpha (TNF-alpha) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1 beta, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3. Conclusion: GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways.
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页数:11
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