论文部分内容阅读
目的:研究替米沙坦对肝硬化患者门静脉的血流动力学及肝纤维化程度的影响及机制。方法:80例肝硬化患者随机分为对照组和治疗组各40例,对照组给予常规治疗,治疗组在此基础上加用替米沙坦80mg.d-1,疗程1个月。2组患者治疗前后应用彩色多普勒超声仪检测门、脾静脉的内径与流速,同时采用放免法检测血降钙素基因相关肽(CGRP)、透明质酸(HA)的水平,酶联免疫法测定血转化生长因子β1(TGFβ1)、血小板源性生长因子(PDGF)的水平,RT-PCR检测过氧化物酶体增生物活化受体γ(PPARγ)mRNA水平。结果:对照组患者治疗后血清PPARγmRNA、CGRP、HA、TGFβ1、PDGF水平以及门、脾静脉的内径与流速无显著性变化(P>0.05)。替米沙坦治疗后,患者血清PPARγmRNA水平升高(P<0.05),CGRP、TGFβ1、PDGF和HA水平下降(P<0.05),门、脾静脉的内径减小,平均流速增快(P<0.05)。结论:替米沙坦不仅可通过阻断血管紧张素Ⅱ的生物活性、上调PPARγ水平,抑制TGFβ1、PDGF表达而发挥抗肝纤维化作用,而且可通过降低血清CGRP水平及抗肝纤维化作用而降低门静脉压力。
Objective: To study the influence of telmisartan on the hemodynamics and the degree of hepatic fibrosis in patients with cirrhosis and its mechanism. Methods: Eighty patients with cirrhosis were randomly divided into control group and treatment group, 40 cases in each group. The control group was given routine treatment. The treatment group was treated with telmisartan 80 mg.d-1 for 1 month. Before and after treatment, the diameters and velocities of portal vein and splenic vein were detected by color Doppler sonography, and the levels of CGRP, HA were detected by radioimmunoassay (TGFβ1) and platelet derived growth factor (PDGF) were measured by ELISA. The mRNA expression of peroxisome proliferator activated receptor γ (PPARγ) was detected by RT-PCR. Results: The levels of PPARγmRNA, CGRP, HA, TGFβ1 and PDGF, as well as the diameters and velocities of portal and splenic veins in control group were not significantly changed after treatment (P> 0.05). After telmisartan treatment, the levels of serum PPARγmRNA and the levels of CGRP, TGFβ1, PDGF and HA in portal vein and splenic vein decreased (P <0.05, P < 0.05). Conclusion: Telmisartan can not only inhibit hepatic fibrosis by blocking the biological activity of angiotensin Ⅱ, up-regulating the level of PPARγ and inhibiting the expression of TGFβ1 and PDGF, but also can reduce the level of serum CGRP and anti-hepatic fibrosis Reduce portal pressure.