Inhibitory effect of lactate on the cell apoptosis via GPR81 after hypoxic-ischemic brain damage
10.12007/j.issn.0258-4646.2025.02.003
- VernacularTitle:缺氧缺血性脑损伤后乳酸通过GPR81抑制细胞凋亡
- Author:
Haochen ZHENG
1
;
Yang ZHENG
1
;
Xiaoming WANG
1
Author Information
1. 中国医科大学附属盛京医院放射科,沈阳 110004
- Publication Type:Journal Article
- Keywords:
hypoxia-ischemia;
G protein-coupled receptor 81;
apoptosis;
lactate
- From:
Journal of China Medical University
2025;54(2):109-114
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe changes in the lactate(Lac)receptor,G protein-coupled receptor 81(GPR81),and apoptosis after hypoxic ischemic brain injury in newborn piglets,and to clarify the mechanism of Lac/GPR81 signal pathway on the cell apoptosis through the intervention of Lac.Methods Thirty newborn piglets were selected.A total of 21 newborn piglets were randomly divided into Sham and hypoxia-ischemia(HI)model groups,and the HI model group was subdivided into 0-2 h,2-6 h,6-12 h,12-24 h,24-48 h,and 48-72 h HI groups,with n=3 each group.Changes in GPR81 expression and apoptosis in the basal ganglia after HI injury were observed using immunohistochemical and TUNEL staining.Nine newborn piglets were randomly divided into Sham+normal saline(NS),HI+NS,and HI+Lac groups,with n=3 each group.The effects of Lac on the expression of GPR81,apoptotic cell percentage,and the expressions of PI3K,AKT,Bcl-2,and Bax in the basal ganglia after HI injury were observed.Results The cell apoptosis rate increased gradually after HI injury and peaked at 24-48 h(P＜0.05).After HI injury,GPR81 expression initially increased and then decreased,peaking at 2-6 h(P＜0.05).The cell apoptosis rate and the expressions of Bax were higher and p-AKT/AKT ratio and the expressions of PI3K and Bcl-2 were lower in the HI+NS group compared with the Sham+NS group(all P＜0.05).The cell apoptosis rate and the expressions of Bax were lower and p-AKT/AKT ratio and the expressions of GPR81,P13K,and Bcl-2 were higher in the HI+Lac group compared with the HI+NS group(all P＜0.05).Conclusion After HI injury,exogenous Lac can inhibit cell apoptosis through activation of the PI3K/AKT signaling pathway mediated by GPR81.
