红景天苷对人心肌细胞缺氧损伤的保护作用及可能机制

Protective effect of salidroside on human myocardial cells during hypoxia injury and possible mechanism

目的观察人心肌细胞(HCM)在不同浓度红景天苷的刺激下其乳酸脱氢酶(LDH)、脱酸激酶(CK)、谷草转氨酶(AST)和超氧化物歧化酶(SOD)的释放量,以及心肌细胞活性的变化。分析红景天苷对人心肌细胞的作用,并探讨其可能的分子机制。方法体外模拟缺氧环境对人心肌细胞造成损伤,测定不同浓度红景天苷作用下人心肌细胞LDH、CK、AST以及SOD释放量,并采用活细胞计数法试剂盒(cck-8)检测不同处理组细胞活性,赫克斯特-碘化丙啶(Hoechst-PI)双染观察细胞凋亡情况,免疫荧光染色检测低氧诱导因子(HIF-1α)表达。结果与缺氧对照组比较,1×10^(-4)、10^(-5)及10^(-6) mol/L红景天苷处理组LDH、CK和AST释放量均降低,呈剂量依赖性(P<0.01)。与缺氧对照组比较,红景天苷处理组(1×10^(-4)、10^(-5)及10-6 mol/L)细胞上清SOD含量增加,呈剂量依赖性(P<0.01)。与缺氧对照组比较,红景天苷处理组(1×10^(-4)、10^(-5)及10-6 mol/L)人心肌细胞随着红景天苷的剂量增大,细胞活性逐渐升高。与缺氧对照组比较,红景天苷处理组(1×10^(-4)、10^(-5)及10^(-6) mol/L)人心肌细胞随着红景天苷的剂量增大,死亡以及凋亡细胞呈现明显减少趋势。缺氧可激活HIF-1α的表达。结论红景天苷能抑制人心肌细胞LDH、CK和AST的释放,增加SOD的含量,同时可提高人心肌细胞的活性并减少其凋亡,对其有保护作用,其分子机制可能与诱导HIF-1α的表达有关。

Objective To investigate the effect of different concentrations of salidroside on LDH, CK, AST and SOD release quantity in supernatant of human myocardial cells, and the changes of human myocardial cells activity, and To find the effect of salidroside on human myocardial cells and discuss the possible molecular mechanisms. Methods The hypoxic model in vitro was established and the LDH, CK, AST and SOD release quantity in supernatant of human myocardial cells dealt with different concentrations of salidroside were measured. Cell activity of different treatment groups was analyzed by CCK-8 assay. Apoptotic changes in HCM cells were observed by using Hoechst-PI staining. The expression of HIF-1α was determined by immunofluorescence. Results Compared with the hypoxia control group, the concentration of LDH, CK, and AST was significantly decreased and SOD was significantly increased with the dose-dependent dealt by different concentrations of salidroside （1×10^-4, 10^-5 and 10^-6 mol/L）. Salidroside significantly increased the activity of human myocardial cells with the dose-dependent. Compared with the hypoxia control group, human myocardial cell death and apoptotic of salidroside treatmentgroups （1×10^-4, 10^-5 and 10^-6 mol/L） showed significant decreased trend. Hypoxia activated the HIF-1α expression. Conclusions Salidroside could significantly inhibit the release of LDH, CK and AST, and increase SOD content in human myocardial cells. At the same time, it can improve the activity and reduce apoptosis of human myocardial cells. The molecular mechanism may be related to HIF-1α expression.