Protective effect of MOTS-c peptide on myocardial injury in rats with myocardial ischemia reperfusion
10.19405/j.cnki.issn1000-1492.2024.08.017
- Author:
Yu Wang
1
;
Jianye Peng
2
;
Mingyan Zhu
2
Author Information
1. Dept of Laboratory，The Second Affiliated Hospital， Hengyang Medical School，University of South China，Hengyang 421001
2. Dept of Cardiovascular Medicine，The Second Affiliated Hospital， Hengyang Medical School，University of South China，Hengyang 421001
- Publication Type:Journal Article
- Keywords:
MOTS-c peptide;
myocardial ischemia reperfusion;
myocardial injury;
mitochondrial biosynthesis;
peroxisome proliferators-activated receptor γ coactivator l alpha
- From:
Acta Universitatis Medicinalis Anhui
2024;59(8):1405-1410
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate the protective effect of mitochondria-derived peptide MOTS-c on myocardial ischemia reperfusion injury (MIRI) in rats and elucidate its mechanism．
Methods :The SD rats were randomly di- vided into sham group，MIRI group，MOTS-c group and MOTS-c + PGC-1α inhibitor SR-18292 group (MOTS-c + SR-18292) ，with 10 rats in each group． The MIRI model was established by ligating the anterior descending branch of the coronary artery MOTS-c peptide ( 1 mg / kg) ，SR-18292 (20 mg / kg) and equal volume concentration of 1% dimethyl sulfoxide were administered via tail vein at 1 h before operation and immediately after operation．At 24 h after surgery，TTC staining was used to observe myocardial infarction size．HE staining was used to observe the pathological changes of myocardial tissue．TUNEL staining was used to detect myocardial apoptosis．ELISA and biochemical kits were used to measure the levels of myocardial injury markers and oxidation indicators in serum of each group．The relative copy number of mtDNA in myocardial tissues was detected by qRT-PCR. The mitochondri- al biosynthesis-related protein expression levels in myocardial tissues were detected by Western blot.
Results:Compared with sham group，MIRI group had serious myocardial injury，myocardial infarction size and increased ap- optosis level (P＜0. 05) ．The mtDNA relative copy number in myocardial tissue decreased (P＜0. 05) ．The con- tents of CK-MB ，LDH ，cTnI in serum and MDA in myocardial tissue increased (P ＜0. 05 ) ． SOD content and PGC-1α , NRF-1 and TFAM protein expression levels in myocardial tissue decreased (P＜0. 05) ．Compared with MIRI group，myocardial injury in MOTS-c group was significantly improved，myocardial infarction size and apopto- sis level decreased (P＜0. 05) ．The mtDNA relative copy number in myocardial tissue increased (P＜0. 05) ．The contents of CK-MB，LDH，cTnI in serum and MDA in myocardial tissue decreased (P＜0. 05) ．The SOD content and the expression levels of PGC-1α , NRF-1 and TFAM in myocardial tissue increased (P ＜0. 05 ) ． Compared with MOTS-c group ，the myocardial infarction size and apoptosis level of rats in MOTS-c + SR-18292 group in- creased (P＜0. 05) ．The mtDNA relative copy number in myocardial tissue decreased (P＜0. 05) ．The contents of CK-MB，LDH，cTnI in serum and MDA in myocardial tissue increased (P＜0. 05) ．SOD content and PGC-1α , NRF-1 and TFAM protein expression levels in myocardial tissue decreased ( P ＜0. 05 ) ．
Conclusion :MOTS-c peptide can improve myocardial injury in MIRI rats by promoting mitochondrial biosynthesis and inhibiting cardio- myocyte apoptosis，and its mechanism may be related to up-regulation of PGC-1α expression.
- Full text:2024091415120321799MOTS-c肽对心肌缺血再灌注大鼠心肌损伤的保护作用_王毓.pdf
