芝麻素联用维生素E对自发性高血压大鼠心肌细胞凋亡的影响

Effects of sesamin combined with vitamin E on the cardiomyocyte apoptosis of spontaneously hypertensive rats

目的:观察芝麻素(Ses)联用维生素E(Vit E)对自发性高血压大鼠(SHR)心肌细胞凋亡的抑制作用及机制。方法:32只SHR大鼠随机分为SHR组、Ses+Vit E(160 mg·kg^(-1)·d^(-1)+10mg·kg^(-1)·d^(-1))组、Vit E(10 mg·kg^(-1)·d^(-1))及Ses(160 mg·kg^(-1)·d^(-1))组,每组8只,另设WKY正常对照组8只(0. 5%CMC-Na 5 m L/kg)。每天灌胃一次,连续10周。TUNEL法检测心肌细胞凋亡水平;免疫组化法检测Bax、Bcl-2的蛋白表达; Western blot法检测心肌组织Bax、Bcl-2、PUMA的蛋白表达及p53的磷酸化水平。结果:芝麻素联用维生素E可显著降低SHR心肌细胞凋亡率,下调心肌组织Bax、PUMA的蛋白表达及p53磷酸化水平,上调Bcl-2的蛋白表达,提高Bcl-2/Bax比值(P <0. 01)。结论:芝麻素联用维生素E对SHR心肌细胞凋亡具有协同抑制作用,其机制可能与减少SHR心肌组织的PUMA蛋白表达,减少p53磷酸化水平,提高Bcl-2/Bax比值,调节Bax和Bcl-2蛋白表达的平衡有关。

AIM: To observe the inhibitory effect and mechanism of sesamin (Ses) combined with vitamin E (Vit E) on the cardiomyocyte apoptosis of spontaneously hypertensive rats (SHR). METHODS: Thirty-two spontaneously hypertensive rats (SHR) were randomly divided into SHR group, Ses combined with Vit E group (160 mg·kg^-1·d^-1+ 10 mg·kg^-1·d^-1), Vit E group (10 mg·kg^-1·d^-1), Ses group (160 mg·kg^-1·d^-1), 8 in each group. Another 8 Wistar-Kyoto rats were included as control group (0.5% CMC-Na 5 mL/kg). The animals were in tragastrically administrated with Vit E, sesamin and CMC-Na once a day for consecutive 10 weeks. After 10 weeks, the cardiomyocyte apoptosis was detected by TUNEL assay; The expression of Bax, Bcl-2 protein was detected with immunohistochemistry staining; The expression of Bax, Bcl-2, PUMA protein and the phosphorylation of p53 was detected by Western blot. RESULTS: The combination of sesamin with vitamin E significantly reduced the cardiomyocytes apoptosis rate of SHR, down-regulated the expression of Bax, Bcl-2, PUMA protein and the phosphorylation of p53, up-regulated the ratio of Bcl-2/Bax (P<0.01). CONCLUSION: Sesamin combined with vitamin E can synergistically inhibit the cardiomyocytes apoptosis of SHR, of which the potential mechanism may be related to the downregulation of PUMA protein expression and p53 phosphorylation, the regulation of the ratio of Bcl-2/Bax, and the regulation of the balance between Bax and Bcl-2 protein expression.