[Baicalin regulates STIM1-mediated calcium overload and reduces apoptosis of cardiomyocytes induced by lipopolysaccharide].

Objective To investigate the protective effect of Baicalin on apoptosis induced by lipopolysaccharide in H9C2 cardiomyocytes and its possible mechanism. Methods In order to establish apoptosis model of H9C2 cardiomyocytes, H9C2 cardiomyocytes were cultured and divided into four groups: the control group; the baicalin group was treated with baicalin at the final concentration of 10μmol/L for 12 hours; the LPS group was stimulated with LPS at the final concentration of 1 μg/ml for 6 hours; The LPS+baicalin group was stimulated with LPS at the final concentration of 1 μg/ml for 6 hours within treated with baicalin at the final concentration of 10μmol/L for 12 hours. Collecting cell samples, CCK-8 (The Cell Counting Kit-8) was used to detect cell activity, and Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) was used to detect the expression levels of apoptosis. Laser Scanning Confocal Microscopy was used to detect the expression levels of store-operated calcium entry in H9C2 cardiomyocytes. Western blot was used to detect the protein expression levels of STIM1, cleaved-caspase3, Bax and Bcl-2. Fluorogenic quantitative PCR was used to detect the mRNA expression level of STIM1. Results Compared with the control group, LPS-induced H9C2 cardiomyocyte survival rate decreased (P<0.05), the expression level of apoptosis increased (P<0.05), the internal flow of calcium increased (P<0.05), the expression levels of cleaved-caspase3, Bax protein levels increased (P<0.05), Bcl-2 protein level decreased (P<0.05), the expression of STIM1 mRNA and protein level increased (P<0.05). Compared with LPS group, the survival rate of H9C2 cardiomyocytes in baicalin intervention group increased (P<0.05), the expression level of apoptosis decreased (P<0.05), the internal flow of calcium decreased (P<0.05), the expression levels of cleaved-caspase3, Bax protein decreased (P<0.05), and the level of Bcl-2 protein increased (P<0.05), the expression of STIM1 mRNA and protein level decreased (P<0.05). Conclusion Baicalin may alleviate LPS-induced cardiomyocyte apoptosis by alleviating calcium overload, and improve cell survival. Key words: Baicalin; Lipopolysaccharide; Cardiomyocyte; apoptosis; store-poperated calcium entry; Stromal interaction molecule 1