| Abstrakt: |
Objective: To investigate the mechanism of Baicalin on the hypoxic injury of H9c2 cardiomyocytes induced by co-balt chloride (CoCl2). Methods: Cobalt chloride (CoCl2) was used to establish a hypoxic injury model in cardiomyocytes, and different concentrations of Baicalin were added for culturing,respectively. The normoxic culture was set as the control group, and the cobalt chloride cultured H9c2 cardiomyocytes were set as the CoCl2 group. The hypoxic H9c2 cardiomyocytes pretreated with Ba- icalin and/or Y27632 (Rho kinase inhibitor) were set as the CoCl2+Baicalin group, CoCl2+Y27632 group and CoCl2+Baicalin+ Y27632 group. Cell proliferation was assessed using the cytotoxicity assay kit (CCK8) assay,and reactive oxygen species (ROS) levels were detected using a fluorescence method. The activity of superoxide dismutase (SOD) in cardiomyocytes was detected by WST-8. The concentration of propylene glycol (MDA) was determined by TBA method. Meanwhile, the expression of RhoA, ROCK1, ROCK2, TNF-α and IL-1 β were analyzed by Western blot as well. Results : After treatment of H9c2 cells for 24 h, 1 000 μmol/L CoCl2 and 75 μmol/L Baicalin showed better cell viability in the treatment of hypoxic injury of cardiomyocytes. The cell activity of the CoCl2 group was significantly lower than that of the control group, and the pre-protective effect of Baicalin on hypoxia-induced cells could significantly increase the cell activity. Compared with the control group, ROS expression level and MDA content in cardiomyocytes of the CoCl2 group increased,protein expression levels of RhoA, ROCK1, ROCK2, TNF-α and IL-1β up-regulated,and SOD activity decreased. Compared with the CoCl2 group, CoCl2+Baicalin could inhibit the expression of ROS and MDA content, up-regulate SOD activity, and down-regulate the expression levels of RhoA, ROCK1, ROCK2, TNF-α and IL-1β,while adding Y27632(Rho kinase inhibitor) significantly enhanced the protective effect of Baicalin. Conclusion: Ba- icalin could alleviate inflammatory and oxidative stress responses to CoCl2-induced injury in H9c2 cardiomyocytes, and its mecha- nism might be related to the inhibition of ROS-dependent RhoA/ROCK pathway. [ABSTRACT FROM AUTHOR] |
