鹿红方对缺血缺氧心肌细胞SDF-1/CXCR4信号通路的影响

Effects of Luhong Decoction on SDF-1/CXCR4 Signaling Pathway in Ischemic and Hypoxic Cardiomyocytes

目的研究鹿红方对缺血缺氧心肌细胞(CMs)抗凋亡能力的影响,并从SDF-1/CXCR4信号通路探讨其作用机制。方法CMs分至对照组,缺血缺氧模型组以及鹿红方各剂量组。采用CCK-8法测定CMs凋亡情况以考查鹿红方对CMs抗凋亡能力的影响及量效果关系。后将CMs分至对照组、模型组、AMD3100组、鹿红方200μg/mL组以及鹿红方+AMD3100组。各组予相应干预措施后采用Western blotting检测Bax、Bcl-2、SDF-1和CXCR4蛋白表达。结果CCK-8结果显示,鹿红方提高CMs抗凋亡能力具有量效关系。Western blotting结果显示:鹿红方200组与模型组比较,SDF-1和CXCR4的表达显著升高(P<0.001),Bax表达显著降低,Bcl-2表达显著升高,Bax/Bcl-2值显著降低(P<0.001),鹿红方+AMD3100组与鹿红方200组比较,Bax表达显著升高,Bcl-2表达显著降低,Bax/Bcl-2值显著升高(P<0.001)。结论鹿红方可提高缺血缺氧状态下CMs的抗凋亡能力,其机制与上调SDF-1/CXCR4信号通路有关。

Objective:To research the effect of Luhong Decoction on apoptosis resistance of cardiomyocytes(CMs)under sugar/oxygen deprivation and to explore its inhibition mechanism via SDF-1/CXCR4 signal pathway.Methods:CCK-8 method was used to measure the apoptosis of CMs to investigate the effect of Luhong Decoction on the anti-apoptotic ability of CMs and the relationship between the quantity and the effect. CMs were then divided into control group,model group,AMD3100 group,Luhong Decoction 200 μg/mL group and Luhong Decoction200 μg/mL+AMD3100 group. Western blotting was used to detect the protein expressions of Bax,Bcl-2,SDF-1and CXCR4 in each group after corresponding intervention measures. Results:CCK-8 showed that there was dose-effect relationship of Luhong Decoction on anti-apoptosis effect. Western blotting results showed that compared with control group,the expression of SDF-1 and CXCR4 in Luhong Decoction 200 μg/mL group was significant high(P < 0.001);the Bax expression significantly decreased(P < 0.001)in the,and a significant increase of the Bcl-2 expression(P < 0.001)was observed,Bax/Bcl-2 value was also significantly decreased(P < 0.001);in the Luhong Decoction 200 μg/mL +AMD3100 group,compared with Luhong Decoction 200 μg/mL group,there was a significant rise in the Bax expression,a significantly reduced Bcl-2 expression,and a significantly increased Bax/Bcl-2(P < 0.001)Conclusion:Luhong Decoction can improve apoptosis resistance of CMs under ischemic and hypoxic condition partly via SDF-1/CXCR4 signal pathway.