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目的探讨白首乌C21甾苷对慢性心力衰竭(CHF)大鼠心肌的保护作用。方法采用Wistar大鼠建立CHF模型,随机分为4组:CHF模型组,给予等体积0.9%氯化钠注射液灌胃;小剂量组,给予白首乌C21甾苷(0.5 g/kg);中剂量组,给予白首乌C21甾苷(1.0 g/kg);大剂量组,给予白首乌C21甾苷(2.0 g/kg);另设假手术组,给予等体积0.9%氯化钠注射液。3周后进行血流动力学、心脏指数、微血管密度(MVD)测量,分别采用Western blot和Real-Time PCR分析检测基质细胞衍生因子-1(SDF-1)蛋白和SDF-1m RNA的表达。结果白首乌C21甾苷中、大剂量组大鼠的左心室收缩压(LVSP)、平均左心室内压最大上升和下降速率(±dp/dtmax)明显高于CHF模型组,左心室舒张期末压(LVEDP)明显低于CHF模型组,左心室松弛时间常数(Tau)明显短于CHF模型组,且呈剂量依赖性,差异均有统计学意义(均P<0.05);白首乌C21甾苷剂量组大鼠的SDF-1蛋白及m RNA表达均明显高于CHF模型组,且呈剂量依赖性,差异均有统计学意义(均P<0.05)。结论白首乌C21甾苷能有效改善CHF大鼠心功能,同时可促进新生血管形成,其机制可能与促进SDF-1表达有关。
Objective To investigate the protective effect of C21-C21 in the heart of chronic heart failure (CHF) rats. Methods Wistar rats were used to establish CHF model. They were randomly divided into 4 groups: CHF model group, given 0.9% sodium chloride injection by intragastric administration; low dose group, C21 acteoside (0.5 g / kg) Middle-dose group was given C21 aconitine (1.0 g / kg); high-dose group, given Baishuwu C21 acteoside (2.0 g / kg); another set of sham operation group, given an equal volume of 0.9% sodium chloride Injection. After 3 weeks, hemodynamics, cardiac index and microvessel density (MVD) were measured. The expression of SDF-1 and SDF-1mRNA were detected by Western blot and Real-Time PCR respectively. Results The left ventricular systolic pressure (LVSP) and mean left ventricular pressure (± dp / dtmax) were significantly higher in middle and high dose CBS group than those in CHF model group. The left ventricular end diastolic dimension (LVEDP) was significantly lower than CHF model group, the left ventricular relaxation time constant (Tau) was significantly shorter than the CHF model group, and in a dose-dependent manner, the differences were statistically significant (P <0.05) Compared with CHF model group, SDF-1 protein and mRNA expression of SDF-1 protein in the dose of glycosides group were significantly increased (all P <0.05). Conclusion C21-C21 can improve cardiac function of CHF rats and promote neovascularization. Its mechanism may be related to the promotion of SDF-1 expression.