Protective Effect and Mechanism of Ginsenosides CK on Rat's Myocardial Ischemia Reperfusion Injury

XUN Ping; SUN Li

doi:10.13422/j.cnki.syfjx.2016160155

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Protective Effect and Mechanism of Ginsenosides CK on Rat's Myocardial Ischemia Reperfusion Injury

更新时间：2024-01-04

- Protective Effect and Mechanism of Ginsenosides CK on Rat's Myocardial Ischemia Reperfusion Injury
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 22, Issue 16, Pages: 155-158(2016)
- 作者机构：
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- DOI：10.13422/j.cnki.syfjx.2016160155
  CLC： R285.5
- Published：2016
- 稿件说明：
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XUN Ping, SUN Li. Protective Effect and Mechanism of Ginsenosides CK on Rat's Myocardial Ischemia Reperfusion Injury[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(16): 155-158.
DOI：

XUN Ping, SUN Li. Protective Effect and Mechanism of Ginsenosides CK on Rat's Myocardial Ischemia Reperfusion Injury[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(16): 155-158. DOI： 10.13422/j.cnki.syfjx.2016160155.

摘要

目的：探讨人参皂苷CK对大鼠心肌缺血再灌注损伤的保护作用及潜在机制。方法： SD大鼠随机均分为5组，分别为假手术组及缺血再灌注模型组给予生理盐水、人参皂苷CK低、中、高剂量组（10，20，40 mg·kg-1），每组12只，ip人参皂苷CK，14 d后，行在体结扎冠状动脉前降支手术30 min后，再进行120 min灌注，复制心肌缺血再灌注大鼠模型，检测人参皂苷CK对心肌梗死面积，血清乳酸脱氢酶（LDH），肌酸磷酸激酶（CPK），诱导型一氧化氮合酶（iNOS），白细胞介素-6（IL-6），肿瘤坏死因子-α（TNF-α）水平，心肌组织丙二醛（MDA）含量，超氧化物歧化酶（SOD）活性及高迁移率族蛋白1（HMGB1）蛋白表达的影响。结果：与正常组比较，缺血再灌注模型组心肌组织MDA含量明显升高，SOD活性明显降低，血清中iNOS，IL-6和TNF-α水平明显升高，心肌组织HMGB1蛋白的表达明显升高（P<0.05）；与缺血再灌注模型组比较，人参皂苷CK能够明显减少心肌梗死面积，降低LDH，CPK活性减少心肌组织MDA含量，提高SOD活性，明显降低血清中iNOS，IL-6和TNF-α水平（P<0.05），此外，人参皂苷CK能够抑制心肌组织HMGB1蛋白的表达（P<0.05）。结论：人参皂苷CK对大鼠心肌缺血再灌注损伤具有一定的保护作用，该作用与其提高机体抗氧化能力、减少炎症反应及抑制HMGB1表达有关。

Abstract

Objective: To discuss the protective effect and potential mechanism of ginsenosides CK on rat's myocardial ischemia reperfusion injury (MIRI). Method: SD rats were randomly divided into 5 groups:sham-operated group

MIRI group (normal saline) and ginsenosides CK low

medium and high-dose groups (10

40 mg·kg-1). Ginsenosides CK was intraperitoneally injected for 14 days. the anterior descending coronary artery was ligated; 30 min later

reperfusion was performed for 120 min to establish the reperfusion model. Effects of ginsenosides CK on infarct area

levels of serum lactic denydrogenase(LDH)

creatine phosphokinase(CPK)

inducible nitric oxide synthase(iNOS)

interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α)

and malondialdehyde(MDA) content

super oxide dismutase(SOD) activity and high mobility group box-1(HMBG1) expression were investigated. Result: Compared with the normal group

the MIRI group showed significant increase in MDA content in myocardia

serum iNOS

IL-6 and TNF-α levels

and HMGB1 protein in myocardia

and significant decrease in SOD activity (P<0.05). Ginsenosides CK could reduce the infarct size and activities of LDH and CPK compared with those in the MIRI group (P<0.05). Ginsenosides CK could lessen the MDA contents and SOD activity of cardiac muscle tissues compared with those in the MIRI group (P<0.05). Ginsenosides CK could lower the levels of iNOS

IL-6 and TNF-α compared with those in the MIRI group (P<0.05). Meanwhile

Ginsenosides CK could inhibit the expression of HMBG1 compared with those in the MIRI group (P<0.05). Conclusion: Ginsenosides CK has a certain protective effect on myocardial ischemia-reperfusion injury in rats

and its effect is related to the enhancement in antioxidant capacity

the reduction of inflammation and the inhibition of the HMBG1 expression.

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