Shuangshen Ningxin Capsules Regulates Mitochondrial Fission and Fusion to Alleviate Myocardial Ischemia-reperfusion Injury in Rats
10.13422/j.cnki.syfjx.20231316
- VernacularTitle:双参宁心胶囊调控线粒体分裂、融合减轻大鼠心肌缺血再灌注损伤
- Author:
Gaojie XIN
1
;
Yuanyuan CHEN
1
;
Zixin LIU
1
;
Yue YOU
1
;
Ce CAO
1
;
Aoao WANG
1
;
Hongxu MENG
1
;
Xiao HAN
1
;
Jianxun LIU
1
;
Lei LI
1
;
Jianhua FU
1
Author Information
1. Institute of Basic Medicine， Xiyuan Hospital， China Academy of Chinese Medical Sciences， Beijing 100091， China
- Publication Type:Journal Article
- Keywords:
Shuangshen Ningxin capsules;
mitochondrial fission;
mitochondrial fusion;
myocardial ischemia-reperfusion injury
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(7):87-94
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore whether the mechanism of Shuangshen Ningxin capsules （SSNX） in alleviating myocardial ischemia-reperfusion injury （MIRI） in rats is related to the regulation of mitochondrial fission and fusion. MethodThis study focused on Sprague Dawley （SD） rats and ligated the left anterior descending branch of the coronary artery to construct a rat model of MIRI. The rats were divided into the sham operation group， model group， SSNX group （90 mg·kg-1） and trimetazidine group （5.4 mg·kg-1）. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） were detected by micro method. Changes in mitochondrial membrane potential （△Ψm） and the degree of mitochondrial permeability transition pore （mPTP） opening were detected by the chemical fluorescence method. The intracellular adenosine triphosphate （ATP） level was detected by the luciferase assay. The messenger ribonucleic acid （mRNA） and protein expression levels of mitochondrial fission and fusion related factors dynamin-related protein 1 （DRP1）， mitochondrial fission 1 protein （FIS1）， optic atrophy protein 1 （OPA1）， mitochondrial outer membrane fusion protein 1 （MFN1）， and MFN2 were detected by real-time polymerase chain reaction （real-time PCR） and Western blot. ResultCompared with the sham operation group， the model group showed a decrease in serum SOD activity and an increase in MDA content. The opening level of mPTP， the level of △Ψm and ATP content decreased， the protein expressions of mitochondrial fission factors DRP1 and FIS1 increased， and the protein expressions and mRNA transcription levels of fusion related factors OPA1 and MFN1 decreased. Compared with the model group，SSNX significantly increased serum SOD activity， reduced MDA content， increased intracellular ATP level and △Ψm， reduced the opening level of mPTP， downregulated the protein expressions of mitochondrial fission factors DRP1 and FIS1， and increased the mRNA transcription levels and protein expressions of fusion related factors OPA1 and MFN1. ConclusionSSNX inhibits the expressions of mitochondrial fission factors DRP1 and FIS1， and increases the expressions of fusion related factors OPA1 and MFN1， inhibiting mitochondrial fission and increasing mitochondrial fusion， thereby alleviating MIRI.
