医学分子生物学杂志 ›› 2023, Vol. 20 ›› Issue (6): 473-478.doi: 10.3870/j.issn.1672-8009.2023.06.002

• 论著 • 上一篇    下一篇

氧化槐果碱对心肌缺血再灌注损伤大鼠的保护作用及机制 #br#

  

  1. 联勤保障部队第九八医院检验输血科 南昌市, 330002
  • 出版日期:2023-11-30 发布日期:2023-12-28
  • 基金资助:
    江西省科技厅自然科学基金 (No. 20192BAB205087), 江西省卫健委课题项目 (No. 202131117)

Protective Effect of Oxysophocarpine on Myocardial Ischemia-reperfusion Injury in Rats and Its Mechanism #br#

  1. Department of Laboratory and Blood Transfusion, No. 908 Hospital of Joint Logistics Support Force, Nanchang, 330002, China
  • Online:2023-11-30 Published:2023-12-28

摘要: 目的 探究氧化槐果碱 (oxysophocarpine, OSC) 对大鼠 MIRI 的保护作用及其作用机制方法 超声心动图仪检测心脏功能指标; HE 染色观察心肌组织病变; ELISA 法检测心损标记物及血清炎症因子水平; 试剂盒检测氧化应激标记物; 蛋白质印迹检测相关蛋白表达水平 结果 sham 组相比, I / R 组大鼠出现明显心肌损伤, 心脏功能明显降低, CK-Mb、 Mb cTnI 水平显著上调; 血清 SOD 水平明显降低, MDA LDH 水平升高; TNF-α、 IL-1β、 IL-6 IL-10 水平均明显升高, p-ERK1 / 2 p-JNK 表达显著上调I / R 组相比, OSC 处理后明显改善心肌损伤和心肌功能; 抑制心肌氧化应激和促炎性因子释放; 下调 pERK1 / 2 p-JNK 表达结论 OSC 可改善大鼠 I / R 导致的心脏功能障碍, 并抑制氧化应激和炎症反应,其作用机制与 ERK / JNK 通路下调有关

关键词:

心肌, 缺血再灌注, 氧化槐果碱, 氧化应激, 炎症反应, ERK1 / 2 / JNK1 / 2 磷酸化

Abstract: Objective To explore the protective effect of Oxysophocarpine (OSC) on myocardial ischemia-reperfusion injury in rat and the mechanism. Methods The cardiac function indicators were detected using echocardiography. The myocardial tissue lesions were observed using HE staining. The levels of heart injury markers and serum inflammatory factor were detected using ELISA methods. The oxidative stress markers were detected using corresponding reagent kits. Theexpression levels of related proteins were detected using Western bloting. Results Compared withthe sham group, the I / R group showed obvious myocardial injury, reduced cardiac function, and up-regulated levels of CK-Mb, Mb and cTnI. The serum level of SOD was significantly decreased, while that of MDA and LDH were increased. The levels of TNF-α, IL-1β, IL-6 and IL-10 were significantly increased, and the expression levels of p-ERK1 / 2 and p-JNK were significantly up-regulated. Compared with the I / R group, OSC treatment significantly improved myocardial injury and myocardial function. OSC treatment significantly inhibited myocardial oxidative stress and the release of pro-inflammatory factors. OSC treatment decreased p-ERK1 / 2 and p-JNK expressions.Conclusion OSC could improve cardiac dysfunction caused by I / R in rats, and inhibit oxidativestress and inflammatory responses. Its mechanism is related to the downregulation of ERK / JNK pathway.

Key words:

myocardium ischemia-reperfusion, oxysophocarpine, oxidative stress, inflammatory response, ERK1 / 2 / JNK1 / 2 phosphorylation

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