AIM To investigate effect of losartan,an AT1receptor antagonist,on hepatic fibrosis induced byCCl<sub>;</sub>and to determine whether or not AT1receptors are expressed on hepatic stellate cells,METHODS AND...AIM To investigate effect of losartan,an AT1receptor antagonist,on hepatic fibrosis induced byCCl<sub>;</sub>and to determine whether or not AT1receptors are expressed on hepatic stellate cells,METHODS AND RESULTS Fifty male Sprague-Dawley rats,weighing（180±20）g,wererandomized into five groups（control group,modelgroup,and three losartan treated groups）,inwhich all rats were given the subcutaneousinjection of 40% CCl<sub>4</sub>（every 3 days for 6 weeks）except for rats of control group.Rats of losartan-treated groups were treated with losartan（20 mg/kg,10 mg/kg,5 mg/kg,daily gavage）,After 6weeks liver tissue and serum samples of all ratswere examined.Serum hyaluronic acid（HA）,procollagen typeⅢ（PCⅢ）were detected byradioimmunoassays,van Giesion collagen stainingwas used to evaluate the extracellular matrix of ratswith liver fibrosis.The expression of AT1receptors,transforming growth factor-beta（TGF-β）,and alpha-smooth muscle actin（a-SMA）inliver tissue were determined byimmunohistochemical techniques.Compared withmodel group,serum ALT and AST of losartan-treated groups were significantly reduced（t=4.20,P【0.01 and t=4.57,P【0.01）.Serum HAand PCⅢalso had significant differences（t=3.53,P【0.01 and t=2.20,P【0.05）.Thedegree of fibrosis was improved by losartan and correlated with the expressions of AT1 receptors,TGF-β,and α-SMA in liver tissue.CONCLUSION AT1 receptor antagonist,losartan,could limit the progression of the hepatic fibrosisinduced by CCl<sub>4</sub>.The mechanism may be related tothe decrease in the expression of AT1 receptorsand TGF-β,ameliorating the injury of hepatocytes;activation of local renin-angiotensin system mightrelate to hepatic fibrosis;and during progressionof fibrosis,activated hepatic stellate cells mightexpress AT1 receptors.展开更多
目的:探讨左旋氨氯地平联合氯沙坦治疗2型糖尿病肾病(T2DN)合并高血压的疗效及对血压和肾功能的影响。方法:采用随机数字表法将2010年1月至2013年1月本院门诊及住院部收治的260例T2DN合并高血压患者分为实验组和对照组,每组患者130例,...目的:探讨左旋氨氯地平联合氯沙坦治疗2型糖尿病肾病(T2DN)合并高血压的疗效及对血压和肾功能的影响。方法:采用随机数字表法将2010年1月至2013年1月本院门诊及住院部收治的260例T2DN合并高血压患者分为实验组和对照组,每组患者130例,实验组给予左旋氨氯地平和氯沙坦口服联合治疗,对照组仅给予左旋氨氯地平口服治疗,对比两组疗效,并观察两组治疗前后的收缩压(SBP)和舒张压(DBP)、血肌酐(Scr)水平、尿微量白蛋白(UMALB)/尿肌酐(Ucr)水平和24 h UMALB水平。结果:实验组的总有效率90.77%显著高于对照组的78.46%(P<0.05);治疗后两组SBP、DBP、脉压差、SCr、UMALB/Ucr及24h UMALB水平均有显著下降(P<0.05),且实验组均显著低于对照组(P<0.05)。结论:左旋氨氯地平联合氯沙坦不仅可有效降低T2DN合并高血压患者血压,还可有效减少尿液中蛋白的排放,保护患者的肾脏功能,疗效显著,值得推广。展开更多
AIM To assess the effect of ACE inhibitor andAng Ⅱ type Ⅰ（AT1）receptor antagonist inpreventing hepatic fibrosis caused by CCl<sub>4</sub>administration in rats;to investigate whether ornot there are ex...AIM To assess the effect of ACE inhibitor andAng Ⅱ type Ⅰ（AT1）receptor antagonist inpreventing hepatic fibrosis caused by CCl<sub>4</sub>administration in rats;to investigate whether ornot there are expression of AT 1 receptors onhepatic stellate cells;and to observe the effectof Ang Ⅱ on proliferation and ECM synthesis ofcultured HSCs.METHODS Studies were conducted in maleSprague-Dawley rats.Except for thehepatofibrotic model group and the controlgroup,in three treated groups,either enalapril（5 mg/kg）,or Iosartan（10 mg/kg）,or enalapril+Iosartan were given to the fibrotic rats bydaily gavage,and saline vehicle was given tomodel and normal control rats.After 6 weeks,liver fibrosis was assessed directly by hepaticmorphometric analysis,which has beenconsidered the gold standard for thequantification of fibrosis.The expressions of AT1 receptors and（α-mooth muscle actin,α-SMA）in liver tissue or isolated hepatic stellate cells（HSCs）were detected by immunohistochemicaltechniques.The effect of Ang Ⅱ on HSCproliferation was determined by MTT method.Effect of Ang Ⅱ on collagen synthesis of HSCswas determined by <sup>3</sup>H-proline incorporation.RESULTS Contrasted to the fibrosis in rats ofthe model group,groups of rats treated with either enalapril or Iosartan,or a combination oftwo drugs showed a limited expansion of theinterstitium（4.23±3.70 vs 11.22±4.79,P【0.05）,but no difference was observedamong three treated groups（5.38±3.43,4.96±2.96,4.23±2.70,P】0.05）.Expression of AT 1receptors was found in fibrotic interstitium offibrotic rats,whereas in normal control rats theywere limited to vasculature only to a very slightdegree.AT 1 receptors were also expressed onactivated HSCs in the culture.At concentrationsfrom 10<sup>-9</sup>to 10<sup>-5</sup>mol/L,Ang Ⅱ stimulated HSCproliferation in culture in a dose-dependentmanner.Increasing Ang Ⅱ concentrationsproduced corresponding increases in <sup>3</sup>H-prolineincorporation.Differences among groups were significant.CONCL展开更多
文摘AIM To investigate effect of losartan,an AT1receptor antagonist,on hepatic fibrosis induced byCCl<sub>;</sub>and to determine whether or not AT1receptors are expressed on hepatic stellate cells,METHODS AND RESULTS Fifty male Sprague-Dawley rats,weighing（180±20）g,wererandomized into five groups（control group,modelgroup,and three losartan treated groups）,inwhich all rats were given the subcutaneousinjection of 40% CCl<sub>4</sub>（every 3 days for 6 weeks）except for rats of control group.Rats of losartan-treated groups were treated with losartan（20 mg/kg,10 mg/kg,5 mg/kg,daily gavage）,After 6weeks liver tissue and serum samples of all ratswere examined.Serum hyaluronic acid（HA）,procollagen typeⅢ（PCⅢ）were detected byradioimmunoassays,van Giesion collagen stainingwas used to evaluate the extracellular matrix of ratswith liver fibrosis.The expression of AT1receptors,transforming growth factor-beta（TGF-β）,and alpha-smooth muscle actin（a-SMA）inliver tissue were determined byimmunohistochemical techniques.Compared withmodel group,serum ALT and AST of losartan-treated groups were significantly reduced（t=4.20,P【0.01 and t=4.57,P【0.01）.Serum HAand PCⅢalso had significant differences（t=3.53,P【0.01 and t=2.20,P【0.05）.Thedegree of fibrosis was improved by losartan and correlated with the expressions of AT1 receptors,TGF-β,and α-SMA in liver tissue.CONCLUSION AT1 receptor antagonist,losartan,could limit the progression of the hepatic fibrosisinduced by CCl<sub>4</sub>.The mechanism may be related tothe decrease in the expression of AT1 receptorsand TGF-β,ameliorating the injury of hepatocytes;activation of local renin-angiotensin system mightrelate to hepatic fibrosis;and during progressionof fibrosis,activated hepatic stellate cells mightexpress AT1 receptors.
文摘目的:探讨左旋氨氯地平联合氯沙坦治疗2型糖尿病肾病(T2DN)合并高血压的疗效及对血压和肾功能的影响。方法:采用随机数字表法将2010年1月至2013年1月本院门诊及住院部收治的260例T2DN合并高血压患者分为实验组和对照组,每组患者130例,实验组给予左旋氨氯地平和氯沙坦口服联合治疗,对照组仅给予左旋氨氯地平口服治疗,对比两组疗效,并观察两组治疗前后的收缩压(SBP)和舒张压(DBP)、血肌酐(Scr)水平、尿微量白蛋白(UMALB)/尿肌酐(Ucr)水平和24 h UMALB水平。结果:实验组的总有效率90.77%显著高于对照组的78.46%(P<0.05);治疗后两组SBP、DBP、脉压差、SCr、UMALB/Ucr及24h UMALB水平均有显著下降(P<0.05),且实验组均显著低于对照组(P<0.05)。结论:左旋氨氯地平联合氯沙坦不仅可有效降低T2DN合并高血压患者血压,还可有效减少尿液中蛋白的排放,保护患者的肾脏功能,疗效显著,值得推广。
文摘AIM To assess the effect of ACE inhibitor andAng Ⅱ type Ⅰ（AT1）receptor antagonist inpreventing hepatic fibrosis caused by CCl<sub>4</sub>administration in rats;to investigate whether ornot there are expression of AT 1 receptors onhepatic stellate cells;and to observe the effectof Ang Ⅱ on proliferation and ECM synthesis ofcultured HSCs.METHODS Studies were conducted in maleSprague-Dawley rats.Except for thehepatofibrotic model group and the controlgroup,in three treated groups,either enalapril（5 mg/kg）,or Iosartan（10 mg/kg）,or enalapril+Iosartan were given to the fibrotic rats bydaily gavage,and saline vehicle was given tomodel and normal control rats.After 6 weeks,liver fibrosis was assessed directly by hepaticmorphometric analysis,which has beenconsidered the gold standard for thequantification of fibrosis.The expressions of AT1 receptors and（α-mooth muscle actin,α-SMA）in liver tissue or isolated hepatic stellate cells（HSCs）were detected by immunohistochemicaltechniques.The effect of Ang Ⅱ on HSCproliferation was determined by MTT method.Effect of Ang Ⅱ on collagen synthesis of HSCswas determined by <sup>3</sup>H-proline incorporation.RESULTS Contrasted to the fibrosis in rats ofthe model group,groups of rats treated with either enalapril or Iosartan,or a combination oftwo drugs showed a limited expansion of theinterstitium（4.23±3.70 vs 11.22±4.79,P【0.05）,but no difference was observedamong three treated groups（5.38±3.43,4.96±2.96,4.23±2.70,P】0.05）.Expression of AT 1receptors was found in fibrotic interstitium offibrotic rats,whereas in normal control rats theywere limited to vasculature only to a very slightdegree.AT 1 receptors were also expressed onactivated HSCs in the culture.At concentrationsfrom 10<sup>-9</sup>to 10<sup>-5</sup>mol/L,Ang Ⅱ stimulated HSCproliferation in culture in a dose-dependentmanner.Increasing Ang Ⅱ concentrationsproduced corresponding increases in <sup>3</sup>H-prolineincorporation.Differences among groups were significant.CONCL
文摘目的评价氯沙坦钾与坎地沙坦酯治疗原发性高血压合并高尿酸血症的临床疗效。方法 80例原发性高血压合并高尿酸血症患者随机分为试验组40例和对照组40例,试验组口服氯沙坦钾50 mg·d-1,对照组口服坎地沙坦酯8 mg·d-1,2组疗程均为8周,比较2组患者治疗前后血尿酸和血压变化。结果与治疗前比较,试验组和对照组治疗后收缩压和舒张压的下降幅度分别为18.95/12.70 mm Hg和27.18/13.03 mm Hg,差异有统计学意义(P<0.05)。试验组降压总有效率为92.5%,对照组总有效率为95.0%,差异无统计学意义(P>0.05)。试验组治疗后血尿酸水平为(431.98±56.11)μmol·L-1,较治疗前的(495.29±51.04)μmol·L-1明显降低(P<0.05)。对照组治疗前后血尿酸水平(486.79±60.81),(470.66±79.36)μmol·L-1差异无统计学意义(P>0.05)。试验组治疗前后血尿酸水平变化与收缩压水平变化呈正相关(r=0.366,P<0.05)。结论氯沙坦钾对原发性高血压伴高尿酸血症患者降压和降尿酸效果显著。
