氯化锂对高糖致乳鼠心肌细胞损伤的保护作用及其机制

Protective effects of lithium on neonatal rat cardiomyocytes exposed to high glucose

目的:观察不同浓度氯化锂(LiCl)对高糖环境培养下乳鼠心肌细胞的影响,探讨经典Wnt信号途径对高糖致乳鼠心肌细胞损伤的保护作用。方法:40只1～3dSD乳鼠,原代心肌细胞培养后,随机分为对照组、高糖损伤组、氯化锂5、10mmol.L-1组。倒置显微镜下观察心肌细胞形态学改变,TUNEL法检测心肌细胞凋亡,免疫细胞化学方法检测心肌细胞磷酸化糖原合成酶激酶-3β(p-GSK-3β)、β-连环蛋白(β-catenin)的表达变化。结果:与高糖损伤组比较,LiCl5、10mmol.L-1组心肌细胞的搏动频率趋于正常,心肌细胞的凋亡减少(P<0.05),p-GSK-3β和β-catenin的表达增多(P<0.05)。随着LiCl浓度的增加,p-GSK-3β和β-catenin的表达增强。结论:LiCl明显抑制高糖致乳鼠心肌细胞的损伤,该效应可能与经典Wnt信号途径的激活有关。

Objective To investigate the effects of different concentrations of lithium（LiCl） on neonatal rat cardiomyocytes exposed to high glucose,and study the protective effects of canonical Wnt signaling pathway.Methods The ventricular myocardium of neonatal rats about 1-3 d old was obtained.Then the primary culture cardiomyocytes were randomly divided into 4 groups：control group,high glucose damaged group,LiCl 5 and 10 mmol·L-1 group.The morphological of cardiomyocytes were observed by inverted microscope,the apoptotic cardiomyocytes were tested by terminal deoxynucleotidyl transferase mediated dUTP_biotin nick end labeling（TUNEL）,immunocytochemistry staining was used to detect the protein experssions p-GSK-3β and β-catenin.Results Compared with high glucose damaged group,the pulsation frequency of cardiomyocytes tended towards nomal,the apoptotic cardiomyocytes were decreased（P〈0.05）,the expressions of p-GSK-3β and β-catenin were increased（P〈0.05）with the increasing of the concentration of LiCl in LiCl 5 and 10 mmol·L^-1 groups.Conclusion LiCl can significantly inhibit the injury of cardiomyocytes induced by high glucose,its mechanism may be related to the activation of canonical Wnt signaling pathway.