丹皮酚对高血压病血瘀证患者血清干预的人脐静脉内皮细胞膜联蛋白V与肌动蛋白结合的影响

Influence of paeonol on integrating expression of annexin V and actin in human umbilical vein endothelia cell intervened with serum of hypertension patients with syndrome of blood stasis

目的:研究丹皮酚对高血压病血瘀证患者血清损伤后的血管内皮细胞(VEC)的膜联蛋白V与肌动蛋白结合的表达的影响,进一步探讨丹皮酚保护VEC的作用机制。方法:运用CCK-8法检测丹皮酚不同浓度25、50、100、250、500、1 000mg/L对人脐静脉内皮细胞活性的影响;选用250mg/L浓度的丹皮酚预干预细胞模型,运用免疫印记杂交技术检测丹皮酚组与对照组膜联蛋白V与肌动蛋白结合的表达。结果:丹皮酚不同浓度对细胞活性的影响:不同浓度组之间比较,差异无统计学意义。250mg/L丹皮酚干预后对与肌动蛋白结合的膜联蛋白V表达的影响:模型对照组、丹皮酚组与肌动蛋白结合的膜联蛋白V的表达逐渐降低,其中每组与肌动蛋白结合的膜联蛋白V的表达呈现血瘀证组、非血瘀证组、正常组逐渐降低的趋势。血瘀证组,丹皮酚组与模型对照组比较,差异有统计学意义(P<0.05)。结论:丹皮酚具有保护人脐静脉内皮细胞完整性的作用,其机制可能是通过降低肌动蛋白G/F含量比值的方式,减少膜联蛋白V与肌动蛋白的结合,促进肌动蛋白的重装。

Objective： To study the inl uence of paeonol on the integrating expression of annexin V and actin ininjured vein endothelia cell（VEC）intervened with serum of hypertension patients with syndrome of blood stasis, and to investigate the action mechanism of paeonol in protecting VEC deeply. Methods： The inl uence of 25, 50, 100, 250, 500, 1 000mg/L paeonol onthe activity of human umbilical vein endothelia cell（HUVEC） was determined by CCK-8 method. The cell models were intervened with250mg/Lpaeonol, and the integrating expression of annexin V and actin of paeonol group and control group was tested by usingwestern blotting. Results： The inl uence of paeonol with different concentrations as 25, 50, 100, 250, 500, 1 000mg/L in cell activity had no statistical significance. The expression of annexin V integrated with actin of model group and 250mg/L paeonol group was decreased gradually, and the expression of annexin V integrated with actin showed a tendency of gradually decreased in syndrome of blood stasis group and followed by non-syndrome of blood stasis group and control group. The difference among syndrome of blood stasis group, paeonol group and model group had statistical significance（P0.05）. Conclusion： Paeonol could protect the integrity of HUVEC through decreasing the content ration of G/F of action, reducing the combination ofannexin V and actin and promoting the reloading of actin.