目的探讨血管紧张素（-1-7）[Angiotensin（-1-7）,Ang（-1-7）]对血管紧张素Ⅱ（AngiotensinⅡ,AngⅡ）在大鼠心脏成纤维细胞（Cardiac fibroblasts,CFs）中信号转导的影响及其机制。方法原代分离培养并鉴定新生SD大鼠的CFs,将细胞分为8组:空白对照组、AngⅡ组、Ang（-1-7）组、AngⅡ+Ang（-1-7）组、AngⅡ+Ang（-1-7）+A-779组、AngⅡ+Ang（-1-7）+PAO组、Ang（-1-7）+PAO组和AngⅡ+PAO组,Western blot法检测细胞外信号调节激酶1/2（Extracellular signal regulated kinase 1/2,ERK1/2）和磷酸化的ERK1/2（p-ERK1/2）的表达;免疫沉淀捕捉分析法检测蛋白酪氨酸磷酸酶-1（Src-homology domain 2 containing protein tyrosine phosphatase-1,SHP-1）的酶活性;实时荧光定量PCR检测转化生长因子-β1（Transforming growth factor-β1,TGF-β1）、I型胶原蛋白（CollagenⅠ,ColⅠ）和Ⅲ型胶原蛋白（CollagenⅢ,ColⅢ）基因mRNA的转录水平。结果 AngⅡ可增加细胞内p-ERK1/2的表达水平和p-ERK/ERK值（磷酸化的p-ERK1/2与总的ERK1/2的比值）,Ang（-1-7）通过与Mas受体结合可拮抗AngⅡ引起的上述效应;Ang（-1-7）通过与Mas受体结合而激活胞内SHP-1的活性,并可拮抗AngⅡ所致的SHP-1活性降低;抑制SHP-1的活性后,Ang（-1-7）拮抗AngⅡ诱导的p-ERK1/2表达水平和p-ERK/ERK值增高的效应被抑制。Ang（-1-7）对TGF-β1、ColⅠ和ColⅢ基因mRNA的转录水平无显著影响,但可抑制AngⅡ所诱导的上述基因mRNA转录水平的增加。结论 Ang（-1-7）通过与Mas受体结合而激活SHP-1,该效应与Ang（-1-7）拮抗AngⅡ诱导的p-ERK1/2的表达水平和p-ERK/ERK值增高密切相关;Ang（-1-7）可抑制AngⅡ所诱导的TGF-β1、ColⅠ和ColⅢ基因表达上调,这些现象可能体现了一种Ang（-1-7）拮抗AngⅡ所致的不良效应的保护性机制。

OBJECTIVE:To analyze the efficacy and safety of intra-aortic balloon pump (IABP) therapy in patients with acute myocardial infarction(AMI) based on the meta-analysis.METHODS:Eligible published randomized controlled clinical research (RCT) were retrieved in the Pubmed, EMBase, Cochrane, China biological medical literature, Wanfang, VIP and CNKI database from 1980 to April 2, 2012. The analysis was performed with the software of RevMan 5.1.RESULTS:Thirteen RCTs with 1958 patients (AMI with IABP therapy, n = 970,without IABP therapy, n = 988) were included. The 30-day mortality between the two groups was similar (RR = 0.77, 95%CI 0.58-1.03, P = 0.08), but the 30-day mortality in the cardiac shock subgroup was significantly lower in IABP group than in without IABP group (RR = 0.65, 95%CI 0.44-0.97, P = 0.04). The 6-month mortality was significantly lower in IABP group than in without IABP group (RR = 0.72, 95%CI 0.55-0.94, P = 0.02). The incidence of major bleeding was significantly higher in IABP group than in without IABP group (RR = 1.43, 95%CI 1.16-1.75, P < 0.01).CONCLUSION:IABP therapy is effective to reduce earlier mortality post AMI, particularly for patients with cardiac shock.

AIM: To explore the role of placental growth factor(PLGF) in the process of angiotensin Ⅱ(Ang Ⅱ)-induced activation of cardiac fibroblasts(CFs).METHODS: Primary culture and identification of CFs from neonatal Sprague-Dawley rats were performed.The method of fluorescence immunocytochemistry was employed to observe the expression of alpha-smooth muscle actin(α-SMA).Real-time PCR and Western blotting were used to determine mRNA and protein levels.The cell proliferation was observed by WST-1 assay.RESULTS: Compared with control group,the PLGF expression at mRNA and protein levels in Ang II-treated CFs was significantly increased,whereas the mRNA expression of PLGF was decreased in the CFs treated with telmisartan and Ang Ⅱ.Treatment with PLGF induced the proliferation of CFs and increased the protein expression of α-SMA.Treatment with PLGF for 60 min significantly increased the protein levels of p-ERK1/2 in the CFs.Compared with Ang Ⅱ group,the proliferation of CFs was depressed and the protein expression of α-SMA was attenuated in Ang II+anti-PLGF group.The mRNA expression levels of type Ⅰ and type Ⅲ collagens were also down-regulated.CONCLUSION: PLGF might be involved in the process of Ang Ⅱ-induced proliferation of CFs and fibrosis.