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冠心丹参方对大鼠心肌缺血再灌注损伤的保护作用。

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

机构信息

Institute of Medicinal Plant Development - Peking Union Medical College and Chinese Academy of Medical Sciences - Beijing, China.

出版信息

Acta Cir Bras. 2023 Apr 21;38:e380123. doi: 10.1590/acb380123. eCollection 2023.

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.

摘要

目的

心肌缺血/再灌注损伤(MIRI)导致心肌组织坏死,从而增加心肌梗死的面积。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

在大鼠中建立 MIRI 模型;用缺氧复氧法建立大鼠 H9C2 心肌细胞损伤模型。

结果

GXDSF 显著减少心肌缺血面积,减轻心肌结构损伤,降低血清中白细胞介素(IL-1β、IL-6)水平,降低心肌酶活性,增加超氧化物歧化酶(SOD)和还原型谷胱甘肽(GSH)活性,减轻 MIRI 大鼠心肌组织细胞核苷酸结合寡聚化结构域、富含亮氨酸重复和吡咯烷结构域包含的 NOD 样受体家族蛋白 3(NLRP3)、IL-1β、半胱天冬酶-1 和天冬氨酸特异性半胱氨酸蛋白酶 3(GSDMD)的表达。丹酚酸 B 和三七皂苷 R1 可保护 H9C2 心肌细胞免受缺氧再氧合损伤,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 心肌细胞中 NLRP3、IL-1β、半胱天冬酶-1 和 GSDMD 的表达。GXDSF 可减少 MIRI 大鼠的心肌梗死面积,减轻心肌结构损伤,通过降低炎症因子和调控细胞焦亡信号通路,减轻心肌组织炎症和氧化应激。

结论

GXDSF 减轻大鼠 MIRI 心肌梗死损伤,改善心肌缺血损伤的结构损伤,降低心肌组织炎症和氧化应激,其机制可能与调控 NLRP3 有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2710/10129295/9ed4f4e27923/1678-2674-acb-38-e380123-gf01.jpg

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