Role of GPR30 in 17β estradiol-induced inhibition of ketamine-caused neuroapoptosis in hippocampus of newborn rats: the relationship with p-ERK1/2
10.3760/cma.j.issn.0254-1416.2019.08.004
- VernacularTitle: GPR30在17β雌二醇抑制氯胺酮致幼鼠海马神经细胞凋亡中的作用：与p-ERK1/2表达的关系
- Author:
Ruiyuan SHANG
1
;
Jianli LI
;
Junfang RONG
Author Information
1. Department of Anesthesiology, Hebei General Hospital, Shijiazhuang 050051, China(is working on Department of Anesthesiology, Xingtai People′s Hospital, Xingtai 054031, China)
- Publication Type:Journal Article
- Keywords:
Receptors, G-protein-coupled;
Estradiol;
Ketamine;
Apoptosis;
Hippocampus;
Extracellular signal-regulated MAP kinases
- From:
Chinese Journal of Anesthesiology
2019;39(8):911-914
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the role of G protein-coupled receptor 30 (GPR30) in 17β estradiol-induced inhibition of ketamine-caused neuroapoptosis in the hippocampus of newborn rats and the relationship with phosphorylated extracellular signal-regulated kinase 1/2 (p-ERKl/2).
Methods:Twenty-four clean-grade healthy male Sprague-Dawley rats, aged 7 days, weighing 11-18 g, were divided into 4 groups (n=6 each) using a random number table method: control group (group C), ketamine group (group K), 17β estradiol plus ketamine group (group EK), and GPR30 inhibitor G15 plus 17β estradiol plus ketamine group (group G15EK). Ketamine 75 mg/kg (diluted to 0.1 ml in normal saline) was intraperitoneally injected every 24 h for 3 consecutive days in group K. In group EK, 17β estradiol 600 μg/kg was subcutaneously injected and ketamine 75 mg/kg was intraperitoneally injected every 24 h for 3 consecutive days.G15 300 μg/kg and 17β estradiol 600 μg/kg were subcutaneously injected and ketamine 75 mg/kg was intraperitoneally injected every 24 h for 3 consecutive days in group G15EK.The equal volume of normal saline 0.1 ml was intraperitoneally injected instead in group C. The animals were sacrificed at 24 h after the last injection for determination of the expression of cleaved caspase-3, ERK1/2 and phosphorylated ERK1/2(p-ERK1/2) (by Western blot).
Results:There was no significant difference in the expression of ERK1/2 in hippocampus among the four groups (P>0.05). Compared with group C, the expression of cleaved caspase-3 was significantly up-regulated, and the expression of p-ERK1/2 was down-regulated in K and G15EK groups (P<0.05). Compared with group K, the expression of cleaved caspase-3 was significantly down-regulated, and the expression of p-ERK1/2 was up-regulated in group EK (P<0.05). Compared with group EK, the expression of cleaved caspase-3 was significantly up-regulated, and the expression of p-ERK 1/2 was down-regulated in group G15EK (P<0.05).
Conclusion:GPR30 is involved in 17β estradiol-induced inhibition of ketamine-caused neuroapoptosis in the hippocampus of newborn rats, which is related to up-regulating the expression of p-ERKl/2.
