Protective effect of Guanxin Danshen formula on myocardial ischemiareperfusion injury in rats.

IF 1.1 4区 医学 Q3 SURGERY Acta cirurgica brasileira Pub Date : 2023-04-21 eCollection Date: 2023-01-01 DOI:10.1590/acb380123
Lanfang Li, Bo Liu, Min Wang, Jingxue Ye, Guibo Sun
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Abstract

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-1β, 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-1β, 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 α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1β, 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.

Conclusions: 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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冠心丹参方对心肌缺血再灌注损伤的保护作用。
目的:心肌缺血/再灌注损伤(MIRI)导致心肌组织坏死,使心肌梗死面积增大。本研究探讨了冠心丹参方(GXDSF)对大鼠MIRI的保护作用及其机制。方法:建立大鼠MIRI模型;对大鼠H9C2心肌细胞进行缺氧复氧,建立细胞损伤模型。结果:GXDSF能显著减少MIRI大鼠心肌缺血面积,减轻心肌结构损伤,降低血清白细胞介素(IL-1β,IL-6)水平,降低心肌酶活性,提高超氧化物歧化酶(SOD)活性和还原型谷胱甘肽。GXDSF可降低心肌组织细胞中核苷酸结合寡聚结构域、富含亮氨酸重复序列和含有nod样受体家族蛋白3(NLRP3)、IL-1β、胱天蛋白酶-1和gasdermin D(GSDMD)的pyrin结构域的表达。丹酚酸B和三七皂苷R1保护H9C2心肌细胞免受缺氧和复氧损伤,并降低细胞上清液中肿瘤坏死因子α(TNF-α)和IL-6的水平,降低H9C2肌细胞中NLRP3、IL-18、IL-1β、胱天蛋白酶-1和GSDMD的表达。GXDSF可减少心肌梗死面积,减轻MIRI大鼠心肌结构损伤,这可能与NLRP3的调节有关。结论:GXDSF降低大鼠心肌梗死损伤的MIRI,改善心肌缺血损伤的结构损伤,并通过降低炎症因子和控制局灶细胞死亡信号通路来减少心肌组织炎症和氧化应激。
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来源期刊
CiteScore
1.90
自引率
9.10%
发文量
60
审稿时长
3-8 weeks
期刊介绍: Information not localized
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