?-Opioid receptor inhibits serum deprivation-induced apoptosis of neonatal cardiac myocytes through activation of protein kinase C signal transduction pathway
- VernacularTitle:?阿片受体激活对依赖于PKC路径的血清饥饿诱导的心肌细胞凋亡的抑制作用
- Author:
Dapeng WANG
;
Hongxin WANG
;
Bo TANG
;
Xiaochun YU
- Publication Type:Journal Article
- Keywords:
receptors;
opioid;
?;
cell apoptosis;
PKC;
caspase-3
- From:
Chinese Pharmacological Bulletin
1987;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the possible mechanism of ?-opioid receptor inhibiting serum deprivation-induced apoptosis of neonatal cardiac myocytes.Methods Myocardial cells of neonatal rats were cultured in vitro,after 48 h,the medium was changed to serum-free DMEM.The experimental groups were:A:Normal;B: Model;C: Model+DADLE(0.1 ?mol?L-1);D:Model+DADLE(0.1 ?mol?L-1)+naltrindole(10 ?mol?L-1);E:Model+DADLE(0.1 ?mol?L-1)+GF109203X(10 ?mol?L-1);F:Model+DADLE(0.1 ?mol?L-1)+staurosporine(1 ?mol?L-1).The cell viability was determined with MTT colormeteric assay;apoptosis index and the percentage of G0 in cell cycle were determined by flow cytometry;Caspase-3 and PKC signal pathway was investigated by Western blot.Results ?-opioid receptor agonist [D-Ala2,D-Leu5]-enkephalin(DADLE) could significantly inhibit serum deprivationinduced apoptosis of neonatal cardiac myocytes,which increased the survival index of cardiac myocyte,percentage of G2/M in cell cycle and the expression of PKC,decreased the apoptotic index of cardiac myocyte,percentage of G0/G1 in cell cycle and the expression of activate caspase-3.The protective effect of DADLE was obviously blocked by ?-opioid receptor antagonist Naltrindole at 10 ?mol?L-1,the PKC inhibitor GF109203X at 10 ?mol?L-1 and staurosporine at 1 ?mol?L-1,which decreased the survival index of cardiac myocyte,percentage of G2/M in cell cycle and the expression of PKC,increased the apoptotic index of cardiac myocyte,percentage of G0/G1 in cell cycle and the expression of caspase-3.Conclusion These findings suggested that ?-opioid receptor activation might be a potential survival factor against serum deprivation-induced myocardial cell apoptosis and this cardioprotective effect might be via PKC pathway.
