Effect of hydrogen on expression of Drp1 in myocardial mitochondria of septic mice
10.3760/cma.j.issn.0254-1416.2017.09.027
- VernacularTitle:氢对脓毒症小鼠心肌线粒体Drp1表达的影响
- Author:
Yuanyuan ZHANG
1
;
Aili DONG
;
Yanyan WANG
;
Keliang XIE
;
Yonghao YU
Author Information
1. 300052,天津医科大学总医院麻醉科天津市麻醉学研究所
- Keywords:
Hydrogen;
Sepsis;
Myocardial injury;
Mitochondrial proteins
- From:
Chinese Journal of Anesthesiology
2017;37(9):1136-1138
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of hydrogen on the expression of Drp1 in the myocardial mitochondria of septic mice.Methods Fifty-four pathogen-free healthy male ICR mice,aged 6 weeks,weighing 20-25 g,were divided into 3 groups (n=18 each) using a random number table:sham operation group (S group),sepsis group (Sep group) and hydrogen group (H2 group).Sepsis was produced by cecal ligation and puncture in anesthetized mice.The mice inhaled 2％ hydrogen for 1 h starting from 1 and 6 h after operation in group H2.The mice were sacrificed at 1 day after operation,and hearts were removed for microscopic examination of the pathological changes which were scored and for determination of apoptosis in cardiomyocytes.Apoptosis rate was calculated.The myocardial mitochondria were isolated for measurement of respiratory control ratio (RCR) (using a Clark-type electrode),ATP content (by using a bioluminescence technique) and Drp1 expression (by Western blot).Results Compared with group S,the pathological score and apoptosis rate were significantly increased,the RCR and ATP content in mitochondria were decreased,and the expression of Drp1 was up-regulated in Sep and H2 groups (P＜0.05).Compared with group Sep,the pathological score and apoptosis rate were significantly decreased,the RCR and ATP content in mitochondria were increased,and the expression of Drp1 was down-regulated in group H2 (P＜0.05).Conclusion The mechanism by which hydrogen mitigates myocardial injury is related to down-regulating expression of Drp1 in the myocardial mitochondria and improving mitochondrial function in septic mice.
