Coenzyme Q10 Inhibits Hydrogen Peroxide-Induced Mitochondrial Dysfunction in Platelets
10.13471/j.cnki.j.sun.yat-sen.univ（med.sci）.2022.0109
- VernacularTitle:辅酶Q10抑制过氧化氢诱导的血小板线粒体功能紊乱
- Author:
Yi-lin SHI
1
;
Ao-lin YANG
2
;
Rui-jie WANG
2
;
Fu-li YA
3
;
Yan-qiu CHEN
4
;
Yan YANG
1
Author Information
1. School of Public Health， Sun Yat-sen University， Guangzhou 510080， China
2. School of Public Health， Sun Yat-sen University （Shenzhen Campus）， Shenzhen 518106， China
3. School of Public Health， Dali University， Dali 671003， China
4. Guangzhou Women and Children Medical Center， Guangzhou 510623， China
- Publication Type:Journal Article
- Keywords:
coenzyme Q10;
platelet;
mitochondrion;
apoptosis;
reactive oxygen species
- From:
Journal of Sun Yat-sen University(Medical Sciences)
2022;43(1):70-76
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveWe explored the protective effects of coenzyme Q10 （CoQ10） on hydrogen peroxide （H2O2）-induced platelet mitochondrial dysfunction and the underlying mechanisms. MethodsPeripheral venous blood from healthy volunteers was collected to prepare gel-filtered platelet suspension. Gel-filtered platelets were incubated with 100 μmol/L CoQ10 for 50 min followed by 30 min incubation with H2O2 （n≥3 per group）. Mitochondrial membrane potential， phosphatidylserine （PS） exposure ratio and mitochondrial reactive oxygen species （mtROS） were measured by flow cytometry. Concentrations of total cellular ROS and ATP were measured by microplate reader. The phosphorylation level of platelet protein p53 and expression levels of Bcl-2 and Bcl-xL were detected by Western blot. ResultsIn resting platelets， CoQ10 had no effect on mitochondrial function （mitochondrial membrane potential， PS exposure positive rate， intracellular ROS， mtROS， ATP levels， P>0.05）. In the oxidative stress model， H2O2 significantly decreased platelet mitochondrial membrane potential and increase PS exposure in platelets. CoQ10 significantly inhibited the dissipation of mitochondrial membrane potential induced by H2O2 ［（35.76%±3.94）% vs. （21.04%±1.69）%，P <0.05］， without inhibitory effect on PS exposure （P >0.05）. Further mechanism study found that CoQ10 directly inhibited the production of ROS and mtROS induced by H2O2 （P<0.05）， reduced the phosphorylation level of p53 and increased Bcl-2 family expression level （P<0.05） while having no effect on ATP content decrease （P>0.05）. ConclusionCoQ10 inhibits H2O2-induced mitochondrial dysfunction in platelets， by reducing p53 phosphorylation and increasing the expression of Bcl-2 family survival protein.
