厄贝沙坦联合阿魏酸钠治疗早期糖尿病肾病78例

目的 观察厄贝沙坦联合阿魏酸讷治疗糖尿病肾病(DN)的临床疗效.方法 选择近期于我院治疗的DN病人78例,作为观察组,采用厄贝沙坦联合阿魏酸钠进行治疗,与厄贝沙坦治疗对照组进行比较,分析两组治疗后血糖水平及各肾功能指标变化.结果 观察组显效率41.0％,显著高于对照组28.0％(P＜0.05).观察组治疗后空腹血糖(FBG)、收缩压(SBP)、血清肌酐(Scr)、尿白蛋白排泄率(UAER)及尿β2微球蛋白(β2- MG)与治疗前比较均显著下降(P＜0.05),且观察组治疗后Scr、尿β2- MG、UAER下降程度明显优于对照组(P＜0.05).结论 厄贝沙坦联合阿魏酸钠治疗糖尿病肾病具有较好的临床疗效.     

厄贝沙坦联合黄芪注射液对老年糖尿病肾病患者结缔组织生长因子的影响

目的观察厄贝沙坦+黄芪注射液对老年糖尿病肾病(DN)患者的血清及尿液中结缔组织生长因子(CTGF)的影响及临床意义。方法早期DN患者据治疗方案随机分为厄贝沙坦组、黄芪注射组、厄贝沙坦+黄芪注射组和对照组各28例。比较4组治疗疗效、血糖、肾功能相关指标及血清、尿液CTGF水平差异。结果 4组治疗有效率有显著差异(χ2=29.97,P0.01),厄贝沙坦+黄芪组有效率最高;治疗前4组空腹血糖(FPG)、糖化血红蛋白(Hb A1c)、尿微量白蛋白排泄率(UAER)、血肌酐(Scr)、血清CTGF及尿液CTGF水平无统计学差异(P0.05),而治疗后4组FPG(F=10.24,P0.01)、Hb A1c(F=9.873,P0.01)、UAER(F=39.68,P0.01)、Scr(F=13.43,P0.01)、血清CTGF(F=64.24,P0.01)、尿液CTGF(F=49.53,P0.01)均有显著差异,且均为对照组水平最高,厄贝沙坦+黄芪组最低。结论厄贝沙坦联合黄芪注射液能够显著降低DN老年患者的血清、尿液CTGF含量,对于DN的疗效更佳。     

ACE2对糖尿病大鼠肾小球足细胞的影响及厄贝沙坦干预作用的研究

目的 探讨糖尿病大鼠肾组织局部血管紧张素转换酶(ACE)2对肾小球足细胞的影响及厄贝沙坦的干预作用.方法 56只Wistar大鼠经链脲佐菌素诱导糖尿病模型,死亡9只,其余随机分为糖尿病组(n=11)、30 mg/(kg·d)肼屈嗪干预组(n=9)、25 mg/(kg·d)厄贝沙坦干预组(n=9)、50 mg/(kg·d)厄贝沙坦干预组(n=9)、200 mg/(kg·d)厄贝沙坦干预组(n=9),同时设正常对照组(n=7).于造模后第4周开始予肼屈嗪、厄贝沙坦干预,第12周观察24h尿微量白蛋白排泄率(UAER),采用免疫组化技术检测肾组织ACE2的分布和表达情况,免疫组化SP法检测肾小球WT1表达情况,Image.Pro Plus 6.0彩色图像分析系统半定量检测足细胞密度.结果 正常对照组UAER低于糖尿病组和药物干预组[包括肼屈嗪干预组、25 mg/(kg·d)厄贝沙坦干预组、50 mg/(kg·d)厄贝沙坦干预组、200 mg/(kg·d)厄贝沙坦干预组](P＜0.001);药物干预组UAER低于糖尿病组(P＜0.001);所有厄贝沙坦干预组UAER较肼屈嗪干预组显著降低(P ＜0.05);50 mg/(kg·d)厄贝沙坦干预组、200 mg/(kg·d)厄贝沙坦干预组UAER较25 mg/(kg·d)厄贝沙坦干预组明显降低(P＜0.001).肾组织ACE2表达与肾小球足细胞密度呈正相关(r=0.381,P＜0.001),糖尿病组ACE2表达较正常对照组明显降低(P＜0.05),而所有厄贝沙坦干预组显著高于糖尿病组和肼屈嗪干预组(P ＜0.001),厄贝沙坦干预组、肼屈嗪干预组足细胞密度显著高于糖尿病组(P ＜0.001);200 mg/(kg·d)厄贝沙坦干预组高于肼屈嗪干预组、25 mg/(kg·d)厄贝沙坦干预组、50 mg/(kg·d)厄贝沙坦干预组、糖尿病组.结论 肾组织ACE2减少可导致足细胞密度降低,进而引起肾脏损害;而厄贝沙坦可上调肾组织ACE2的表达,增加足细胞密度,发挥降压外的肾脏保护作用,且呈现剂量依赖性.     

厄贝沙坦治疗2型糖尿病伴白蛋白尿患者有效性和安全性——多中心随机双盲对照研究

目的 评估厄贝沙坦治疗2型糖尿病伴白蛋白尿患者的疗效与安全性.方法 采用随机、双盲、安慰剂对照、多中心临床研究方法,8个医院326例受试者随机分配到厄贝沙坦(300 mg/d)组(160例)或安慰剂组(166例),治疗24周.检测尿白蛋白排泄率(UAER)、收缩压、舒张压、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇(LDL-C)和HhA1C水平.结果 厄贝沙坦组UAER与基线相比显著下降(P＜0.01),安慰剂组无明显变化(P＞0.05),两组差异有统计学意义(P＜0.01).在意向治疗(ITT)人群高血压和非高血压患者的收缩压、舒张压均有不同程度下降(P＜0.01),而在符合方案(PP)人群却无明显下降.治疗24周后,厄贝沙坦组的LDL-C水平明显低于安慰剂组(P＜0.01).治疗期间厄贝沙坦组低血压的发生率高于安慰剂组,个别患者出现血钾升高.结论 厄贝沙坦300 mg/d可以有效降低2型糖尿病伴白蛋白尿患者的UAER,其疗效独立于降血压作用之外,并且具有良好的安全性和耐受性.     

舒洛地特对糖尿病大鼠肾脏转化生子因子β1与结缔组织生长因子表达的影响

目的 探讨舒洛地特对糖尿病大鼠肾组织转化生长因子β1(TGF-β1)、结缔组织生长因子(CTGF)表达的影响.方法 将SD雄性大鼠腹腔注射链脲佐菌素(STZ)建立早期糖尿病肾病(DN)模型,成模20只,随机分为DN组、糖尿病肾病治疗组(DNS组),各10只,另有10只为对照组.DNS组予以舒洛地特(10 mg·kg-1·d-1)肌肉注射.8 w后,检测各组大鼠的24 h尿白蛋白定量、体重、肾重、肾肥大指数、血糖、血尿素氮、血肌酐,通过免疫组化及Western 印迹观察肾TGF-β1、CTGF的蛋白表达.结果 DN组大鼠的24 h尿白蛋白定量、肾脏肥大指数在糖尿病早期较对照组明显增加(P＜0.01),而DNS组大鼠较DN组明显减少(P＜0.01).DN组大鼠TGF-β1、CTGF表达较对照组明显增加(P＜0.01),DNS组较DN组明显减弱(P＜0.01).结论 早期应用舒洛地特可降低24 h尿白蛋白,抑制糖尿病大鼠早期肾脏肥大,抑制TGF-β1、CTGF表达.舒洛地特对DN的保护机制可能与抑制肾小球细胞外基质积聚有关.     

糖尿病肾病患者血、尿转化生长因子-β1水平变化及其临床意义

目的探讨不同阶段糖尿病肾病患者血、尿转化生长因子β1(TGFβ1)水平变化及其临床意义。方法依据尿微量白蛋白排泄率(UAER)的不同,将68例2糖尿病患者分为3组,正常白蛋白尿糖尿病组23例,UAER<20μg/min;早期糖尿病肾病组25例,UAER>20～200μg/min;临床糖尿病肾病组20例,UAER>200μg/min。用ELISE法测定血、尿转化生长因子β1水平,并对其临床意义进行分析。结果与正常对照组比较,正常白蛋白尿糖尿病组血TGFβ1水平轻度升高,无显著差异(P>0.05);而早期糖尿病肾病组、临床糖尿病肾病组血TGFβ1水平明显升高(P<0.01);3组糖尿病组尿TGFβ1均较对照组明显升高(P<0.05～0.01)。各组糖尿病患者尿TGFβ1水平与UAER呈正相关(r值分别为0.612,0.572,0.624,P均<0.01)。尿TGFβ1与血肌酐也呈正相关(r值为0.513,P<0.05)。结论尿TGFβ1变化可能更早显示基底膜成份和结构变化,可作为较白蛋白更敏感的糖尿病肾病早期诊断的一个指标。     

舒洛地特联合厄贝沙坦治疗老年糖尿病肾病疗效观察

目的 观察舒洛地特联合厄贝沙坦治疗老年糖尿病肾病的临床疗效.方法 选择糖尿病肾病患者65例,随机分为对照组和治疗组.对照组在常规治疗的基础上加用厄贝沙坦,治疗组在对照组的基础上加用舒洛地特,8周后测定2组病人空腹血糖(FBG)、24h尿蛋白定量、血清光抑素C、三酰甘油(TG)、纤维蛋白原(FIB)的变化.结果 治疗组与对照组光抑素C、24h尿蛋白定量都有所下降,治疗组比对照组下降更为明显(P＜0.05);而TG、FIB只有在治疗组有所下降,明显低于对照组(P＜0.01).结论 舒洛地特联合厄贝沙坦可以更有效地改善老年糖尿病肾病患者的肾功能.     

厄贝沙坦联合低分子肝素治疗糖尿病肾病临床观察

将88例糖尿病肾病(DN)患者随机分为两组,在糖尿病常规治疗基础上,对照组加用厄贝沙坦,观察组加用厄贝沙坦、低分子肝素.比较两组尿白蛋白排泄率(UAER)和凝血功能变化.结果与对照组比较,观察组UAER明显下降(P<0.05),血液高凝状态明显改善(P<0.05).提示DN患者联用厄贝沙坦与低分子肝素,可更好地保护肾脏功能.     

中剂量双重阻断肾素血管紧张素系统对糖尿病肾病大鼠肾小管间质转化生长因子-β1、结缔组织生长因子表达的影响

目的 观察中剂量双重阻断肾素血管紧张素系统对糖尿病肾病(DN)大鼠肾小管间质转化生长因子(TGF)-β1、结缔组织生长因子(CTGF)表达的影响.结果 将链脲佐菌素(STZ)诱导的DN大鼠模型随机分为对照组(A组)、贝那普利组(B组)、贝那普利联合氯沙坦组(C组),B组给予贝那普利10 mg·kg-1·d-1灌胃,C组给予贝那普利5 mg·kg-1·d-1、氯沙坦10 mg·kg-1·d-1灌胃,8 w后免疫组化观察各组肾小管间质TGF-β1、CTGF表达,RT-PCR测定TGF-β1、CTGF mRNA表达.结果 B组、C组大鼠小管间质TGF-β1、CTGF表达及mRNA表达较A组均明显下调(P＜0.01),同时C组与B组比较其表达表达也显著下调(P＜0.05).结论 中剂量贝那普利与氯沙坦联合阻断肾素血管紧张素系统,比单用贝那普利能更有效下调DN大鼠肾小管间质TGF-β1、CTGF的表达.     

TGFβ1和CTGF在非酒精性脂肪性肝炎肝组织中的表达及意义

目的:探讨非酒精性脂肪性肝炎(NASH)患者肝脏转化生长因子β1(TGFβ1)和结缔组织生长因子(CTGF)的表达及二者在脂肪性纤维化发展过程中的相关性.方法:采用HE染色,光镜下观察21例非酒精性脂肪性肝炎组(NASH组)肝组织和10例正常肝组织组标本肝组织的病理改变;RT-PCR及免疫组织化学技术分别检测以上两组标本中TGFβ1和CTGF的表达情况.结果:光镜下非酒精性脂肪性肝炎组出现明显炎症反应和纤维化.免疫组化结果显示非酒精性脂肪性肝炎组肝脏TGFβ1和CTGF的表达显著高于正常肝脏组(109.52±4.50 VS 1 14.47±2.00,117.07±3.60 VS 125.05±3.37,均P＜0.01).NASH组TGFβ1和CTGF mRNA的表达水平升高明显,与对照组比较差异有统计学意义(0.66±0.07 VS 0.46±0.04,0.59±0.08VS 0.41±0.05,均P＜0.05).结论:TGFβ1和CTGF在非酒精性脂肪性肝炎中的表达升高可能参与了脂肪性肝炎向肝纤维化转变,CTGF可能在诊断和治疗非酒精性脂肪性肝炎中扮演重要的作用.     

Pro-inflammatory cytokines are associated with podocyte damage and proximal tubular dysfunction in the early stage of diabetic kidney disease in type 2 diabetes mellitus patients

AimsTo evaluate if there is a link between inflammation (expressed by inflammatory cytokines) and the early stage of diabetic kidney disease (DKD), as shown by markers of podocyte damage and proximal tubular (PT) dysfunction.MethodsIn this study were enrolled 117 type 2 DM patients (36-normoalbuminuria, 42-microalbuminuria, 39- macroalbuminuria), and 11 healthy subjects. Serum and urinary IL-1 alpha, IL-8, IL-18, urinary albumin:creatinine ratio (UACR), eGFR, biomarkers of podocyte damage (podocalyxin, synaptopodin, nephrin) and of PT dysfunction (KIM-1, NAG) were assessed.ResultsIn multivariable regression urinary Il-1 alpha correlated positively with podocalyxin and NAG (p < 0.0001, R²= 0.57); urinary IL-8 correlated directly with synaptopodin, NAG, nephrin, and KIM-1 (p < 0.0001, R² = 0.67); urinary IL-18 correlated directly with synaptopodin, NAG, and nephrin (p < 0.0001, R² = 0.59). Serum IL-1 alpha correlated positively with nephrin, synaptopodin, NAG (P < 0.0001, R² = 0.68); serum IL-8 correlated directly with synaptopodin and NAG (p < 0.0001, R² = 0.66); serum IL-18 correlated directly with NAG, KIM-1, and podocalyxin (p < 0.0001, R²=0.647).ConclusionsPro-inflammatory interleukins are associated with podocyte injury and PT dysfunction in early DKD. These could exert a key role in the pathogenesis of early DKD, before the development of albuminuria.     

Association between transforming growth factor β1 and atrial fibrillation in essential hypertensive patients

Abstract

Background: Transforming growth factor β₁ (TGFβ₁) was one of the main factors for accelerating atrial fibrosis and has been reported with significantly higher level in plasma of the patients with essential hypertension (EH), especially in those with target organ damage. The contribution of TGFβ₁ in the pathogenesis of atrial fibrillation (AF) in EH patients remains unknown. Methods: 75 EH patients with documented AF were divided into the paroxysmal AF group (EH+pAF, n?=?44) or the chronic AF group (EH+cAF, n?=?31), and 37 EH patients with sinus rhythm (SR) were assigned into the EH+SR group. All data including EH duration, blood pressure, lipids, glucose and left atrial diameter (LAD) measured by ultrasonic cardiogram were recorded. The serum levels of TGFβ₁ and connective tissue growth factor (CTGF) were detected, and compared with normal controls (NC group, n?=?36). Results: The serum levels of TGFβ₁ and CTGF in all EH groups were significantly higher than those in the NC group (p?<?0.001, respectively). Among the EH groups, TGFβ₁ and CTGF levels were highest in the cAF group, followed by the pAF and the SR groups (p?<?0.005). However, no significant difference was observed in TGFβ₁ and CTGF levels between the cAF group and the pAF group. The serum TGFβ₁ in AF patients was independently correlated with LAD, the presence of AF, aldosterone, CTGF and age. Conclusion: The serum TGFβ₁ promotes CTGF synthesis and causes left atrial enlargement and remodeling, which is possibly involved in the pathogenesis of AF in EH patients.     

The Role of CTGF in Inflammatory Responses Induced by Silica Particles in Human Bronchial Epithelial Cells

Background

Prolonged exposure to crystalline silica leads to persistent pulmonary inflammation and progressive fibrosis. Connective tissue growth factor (CTGF) has emerged as a potent proinflammatory and profibrotic regulator to participate in a variety of chronic inflammatory diseases. However, the role of CTGF in silica-induced pulmonary inflammation remains poorly understood.

Methods

To explore the effect of CTGF on inflammatory responses caused by silica particles, human bronchial epithelial cells (16HBE) were transfected with CTGF siRNA and exposed to silica particles at concentrations of 0, 12.5, 25, 50, 100 μg/ml for 48 h. Intracellular CTGF mRNA and protein expressions were determined by RT-PCR and Western blotting, respectively. The levels of inflammatory cytokines including IL-8, TNF-α, IL-6, IL-1β, IL-17A and TGF-β₁ were measured by ELISA kits.

Results

Silica particles induce significantly elevated intracellular CTGF mRNA expression in 16HBE cells in a dose-dependent manner when compared with blank control group (P < 0.05). The secretions of IL-8, TNF-α, IL-6 and IL-17A were also significantly increased by silica particles (P < 0.05). After exposure to 25 or 50 μg/ml silica particles, the expression of intracellular CTGF mRNA was significantly inhibited in 16HBE cells when transfected with CTGF siRNA (P < 0.05). The secreted levels of IL-8, TNF-α, IL-6 and IL-17A induced by silica particles were also significantly lower from CTGF siRNA-transfected cells than that from normal 16HBE cells (P < 0.05).

Conclusion

Inhibition of CTGF gene attenuates silica-induced inflammatory responses in bronchial epithelial cells, suggesting that CTGF could be a pivotal regulator in the development of silica-induced inflammation.

     

Histone deacetylase inhibitor suberoylanilide hydroxamic acid alleviates liver fibrosis by suppressing the transforming growth factor-β1 signal pathway

Background: Histone deacetylases(HDACs) inhibitors are new anti-fibrotic drugs that inhibit the activity of hepatic stellate cells. The present study focused on the anti-fibrotic function of HDAC inhibitor suberoylanilide hydroxamic acid(SAHA) by suppressing transforming growth factor-β1(TGF-β1) signaling. Methods: Male Sprague-Dawley rats were used to induce liver fibrosis with carbon tetrachloride(CCl 4) and LX2 cell(human hepatic stellate cell line) was stimulated by TGF-β1. Both animals and cells were treated with SAHA. The Smad7 and connective tissue growth factor(CTGF) mRNA levels were detected by real-time polymerase chain reaction(PCR). Western blotting was used to examine the protein levels of CTGF, Histone H3(H3), Smad7, Smad2/3, Acetyl-Histone H3(AH3), HDAC2, α-smooth muscle actin( α-SMA), HDAC6, p-Smad2/3 and HDAC8. In addition, the TGF-β1 and liver enzyme levels from rat serum were detected. Histopathological changes were examined by hematoxylin and eosin(HE), Sirius red and Masson trichrome staining. The α-SMA expression was detected by immumohistochemical staining. Results: Compared with control group, the TGF-β1 and liver enzyme levels from rat serum, together with the mRNA levels of CTGF and protein levels of CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were elevated in fibrotic rats( P 0.01). But the Smad7 mRNA and AH3 protein levels were notably suppressed in the fibrotic rats( P 0.01). Pathological examination showed the typical changes of liver fibrosis in the fibrotic rats. After the treatment with SAHA, the levels of liver enzymes, TGF-β1, CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were reduced( P 0.01) and Smad7 and AH3 protein contents were elevated in liver fibrotic rats( P 0.01). Moreover, immumohistochemistry showed that SAHA significantly suppressed the α-SMA protein content in fibrotic liver( P 0.01). Conclusion: The HDAC inhibitor SAHA alleviated liver fibrosis by suppressing the TGF-β1 signaling.     

Inhibition and prevention of monosodium urate monohydrate crystal–induced acute inflammation in vivo by transforming growth factor β1

Objective. We investigated the effects of transforming growth factor β1 (TGFβ1) on monosodium urate monohydrate (MSU) crystal-induced acute inflammation in vivo. Methods. One hour after MSU crystal–induced acute inflammation was produced in the rat subcutaneous air pouch model, the effects of recombinant human TGFβ1 (rHuTGFβ1; 10–100 pg/animal) and ultrapure TGFβ1 (UPTGFβ1; 100 and 500 pg/animal) were assessed, based on absolute and differential white blood cell counts in the exudate. The effects of 10 pg of rHuTGFβ1 preincubated with a specific anti-TGFβ antibody, and the effects of coinjection of crystals and rHuTGFβ1, were also studied. Results. UPTGFβ1 and rHuTGFβ1 markedly reduced MSU crystal–induced inflammation. Recombinant human TGFβ1 also reduced inflammation when administered concomitantly with MSU crystals. Moreover, rHuTGFβ1 and UPTGFβ1, injected 1 hour after MSU crystal injection, reduced the inflammatory response in a dose-dependent manner. Injection of rHuTGFβ1 (100 pg/animal) resulted in a >90% reduction in the maximal white blood cell count, achieved 6 hours after crystal injection. Preincubation of rHuTGFβ1 with a specific anti-TGFβ1 antibody significantly (P < 0.01) reversed the inhibitory effect of rHuTGFβ1 on the inflammatory response. Consistent with the regulation of inflammatory cell recruitment into the joint, the percentage of monocytes markedly decreased (P < 0.01) following local injection with rHuTGFβ1 6 hours after MSU crystal injection. Conclusion. Exogenous TGFβ1 prevents and inhibits MSU crystal–induced acute inflammation in vivo. Its role in the self-limitation of gouty attacks deserves consideration, among the various other factors involved.     

Relationships between inflammation,hemodynamic function and RAAS in longstanding type 1 diabetes and diabetic kidney disease

The renin angiotensin aldosterone system (RAAS) is associated with renal disease and inflammation in a diabetes setting, however, little is known about the implicated mechanisms in individuals with long standing diabetes. Accordingly, our aim was to perform an observational study to quantify urinary excretion of inflammatory biomarkers in participants with long standing type 1 diabetes (T1D) (with and without diabetic kidney disease [DKD]) and controls, at baseline and in response to RAAS activation. GFR_INULIN, ERPF_PAH, and 42 urine inflammatory biomarkers were measured in 74 participants with T1D for ≥50 years (21 with DKD and 44 without DKD [DKD resistors]) and 73 healthy controls. Additionally, inflammatory biomarkers were measured before and after an angiotensin II infusion (ANGII, 1 ng?kg^?1?min^?1). Significantly lower urinary excretion of cytokines (IL-18, IL-1RA, IL-8), chemokines (MCP1, RANTES) and growth factors (TGF-α, PDGFAA, PDGFBB, VEGF-A) was observed in participants with T1D at baseline compared to controls. Urinary IL-6 was higher in DKD than in DKD resistors in an exploratory analysis unadjusted for multiple comparisons. In T1D only, lower GFR_INULIN correlated with greater excretion of proinflammatory biomarkers (IL-18, IP-10, & RANTES), growth factors (PDGF-AA & VEGFAA), and chemokines (eotaxin & MCP-1). ANGII increased 31 of 42 inflammatory biomarkers in T1D vs controls (p < 0.05), regardless of DKD resistor status. In conclusion, lower GFR and intra-renal RAAS activation were associated with increased inflammation even after longstanding T1D. The increased urinary IL-6 in patients with DKD requires further investigation to determine whether IL-6 is a candidate protective biomarker for prognostication or targeted therapy in DKD.     

结缔组织生长因子与高血压大鼠心肌纤维化相关性及伊贝沙坦的干预研究

目的探讨结缔组织生长因子(CTGF)在高血压大鼠心肌纤维化发生发展中的作用,以及伊贝沙坦改善高血压所致心室重构和心肌纤维化可能的作用机制。方法20只12周龄雄性自发性高血压大鼠(SHR)随机分为SHR组和伊贝沙坦(IRB)组各10只,IRB组每只大鼠予以伊贝沙坦50 mg.kg-1.d-1灌胃,给药时间12周,同时取10只12周龄雄性Wistar大鼠作为对照组(WKY组),用免疫组织化学的方法对转化生长因子β1(TGF-β1)、CTGF在3组大鼠的左室心肌的分布及表达进行半定量分析;用逆转录-聚合酶链反应检测TGF-β1、CTGF mRNA在心肌表达水平;用MOSSON染色法观察左室心肌胶原形态,图像分析测量胶原容积分数(CVF)和血管周围胶原面积(PVCA)。结果(1)左室重量指数(LVI)、CVF、PVCA在SHR大鼠组明显高于WKY大鼠组(P<0.01);与SHR组比较,伊贝沙坦组则显著降低(P<0.05)。(2)CTGF主要在血管平滑肌和心肌间质中表达,相关分析表明:CTGF与TGF-β1(r=0.562,P<0.05)、CVF(r=0.715,P<0.01)、PVCA(r=0.786,P<0.01)呈正相关;(3)CTGF及其mRNA在SHR组左室心肌中的表达较WKY组明显增强(P<0.05),与SHR组比较,IRB组则明显减少。结论高血压大鼠心室肌CTGF表达增加,伊贝沙坦能抑制高血压大鼠心室肌CGTF表达,且明显改善了高血压心室重构和心肌纤维化。