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目的:观察丹桔胶囊对血管紧张素Ⅱ(AngⅡ)损伤血管内皮功能的保护作用。方法:制备大鼠胸主动脉环,观察丹桔胶囊提取剂对抗AngⅡ引起的胸主动脉环收缩反应;AngⅡ刺激人脐静脉血管内皮细胞(HUVEC)以反转录—聚合酶链反应(RT-PCR)方法检测HUVEC的内皮素(ET-1)mRNA表达水平;蛋白质印迹(Western blot)方法检测HUVEC中细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)和核转录因子κB(nuclear factorκB,NF-κB)的活化情况。结果:AngⅡ引起胸主动脉收缩,丹桔胶囊制剂能显著对抗血管收缩作用,下调AngⅡ刺激所致的HUVEC细胞ET-1 mRNA过度表达,抑制ERK1/2磷酸化,同时对NF-的活化表现出显著的抑制作用。p65位移、IκB-α磷酸化降解,丹桔胶囊上述抑制作用均呈现浓度依赖性。结论:丹桔胶囊抑制AngⅡ对血管内皮功能的损伤,其机制与降低ET-1表达,抑制ERK/NF-κB途径活化有关。
OBJECTIVE: To observe the protective effect of Danjuan Capsule on vascular endothelial function induced by angiotensin II (Ang II) injury. METHODS: Rat thoracic aorta rings were prepared to observe the anti-AngII induced thoracic aortic ring contraction response of rat capsule extracts; AngII stimulated human umbilical vein endothelial cells (HUVEC) by reverse transcription-polymerase chain reaction (RT-PCR). The endothelin (ET-1) mRNA expression of HUVEC was detected by PCR and Western blot. The extracellular signal-regulated kinase (ERK) and nuclear factor kappa B (HUB) were detected by Western blot. NF-κB) activation. RESULTS: Ang II caused contraction of thoracic aorta, Dan Tang Capsules could significantly inhibit vasoconstriction, down-regulated the over-expression of ET-1 mRNA in HUVEC cells induced by AngII stimulation, inhibited ERK1/2 phosphorylation, and showed activation of NF- Significant inhibition. The p65 shift and IκB-α phosphorylation degradation showed that the above inhibitory effects of Dan Tang capsules were concentration-dependent. Conclusion: Danzhu Capsule can inhibit the damage of vascular endothelial function induced by AngII. The mechanism is related to the decrease of ET-1 expression and inhibition of ERK/NF-κB pathway activation.