H2S attenuates sepsis-induced cardiomyopathy by regulating the Xc －/ GPX4 pathway in ferroptosis
10.19405/j.cnki.issn1000-1492.2022.12.019
- Author:
Guodong Cao
1
;
Feifei Deng
2
;
Yuhan Zhao
1
;
Youcheng Zeng
1
;
Liang Lin
1
;
Lichun Guo
1
;
Xiqing Luo
1
;
Yixin Zhang
1
;
Ming Huang
1
;
Qinghong Cheng
1
Author Information
1. The Second Department of Critical Care，The First Affiliated Hospital of Shihezi University School of Medicine，Shihezi 832000
2. Pharmacy School of Shihezi University ，Shihezi 832000
- Publication Type:Journal Article
- Keywords:
sepsis-induced cardiomyopathy;
H2 S;
ferroptosisis;
oxidative stress
- From:
Acta Universitatis Medicinalis Anhui
2022;57(12):1959-1964
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To investigate whether NaHS，a hydrogen sulfide donor，can improve myocardial injury in sepsis by inhibiting oxidative stress and activating the Xc －/ GPX4 signaling pathway in ferroptosis．
Methods :Lipopolysacc-haride(LPS) induced H9c2 in rat cardiomyocytes to form an in vitro model of myocardial injury in sep- sis，which was divided into Control group，LPS group and LPS + NaHS group．The kits were applied to detect the changes of cardiomyocyte viability，Fe2 + ，LDH and CK-MB，determine the levels of oxidative stress indexes GSH and MDA，detect the changes of cellular ROS and mitochondrial membrane potential levels by fluorescent probes， and detect the expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 by Western blot.
Results:Compared with the Control group，H9c2 cell viability decreased，Fe2 + concentration increased ，GSH ，MDA and ROS levels increased，mitochondrial JC-1 monomer increased ，expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 decreased，and cell damage increased after LPS stimulation (P＜0. 05) ．Compared with the LPS group，NaHS attenuated LPS-induced H9c2 cell injury and elevated Fe2 + concentration，decreased the level of LPS-induced oxidative stress in H9c2 cells ，and increased the expression levels of ferroptosis regulatory proteins SLC7A11 and GPX4 (P＜0. 05 ) ．
Conclusion :The mechanism by which NaHS attenuates myocardial injury in sepsis may be related to the inhibition of oxidative stress and activation of the Xc －/ GPX4 signaling pathway in fer- roptosis.
- Full text:2024072221560808457H_2S通过调节铁死亡中X...X4通路减轻脓毒症心肌损伤_曹国栋.pdf
