【摘要】 目的 探討坎地沙坦干預后海仁藻酸（kainic acid，KA）致癇大鼠腎臟細胞外信號調節激酶（ERK1/2）的表達及其變化的機制。 方法 105只雄性Wistar大鼠隨機分為3組:A1-5對照組、B1-5 致癇組、C1-5坎地沙坦組，每組各35只，1-5分別表示癲癇后0、2、6、12及24 h。采用立體定位儀下杏仁核內注射KA方法制備大鼠癲癇模型，于致癇后不同時程，進行灌流固定、腎臟組織的石蠟包埋、切片及免疫，組織化學染色，檢測不同時程腎臟ERK1/2表達的灰度值。 結果 與對照組相比，致癇組及坎地沙坦組腎組織于致癇后2 h ERK1/2表達均開始增加（致癇后2 h ERK1/2，致癲組：20 229.18±2 067.27，坎地沙坦組：16 878.19±2 693.97，對照組:8 054.24±975.90， Plt;0.01），致癇后6 h兩組大鼠腎組織ERK1/2的表達均達到高峰（致癇后6 h ERK1/2，致癇組:39 217.34±4 443.33，坎地沙坦組：31 924.85±4 383.80，對照組：8 575.24±1 040.82， Plt;0.01），隨后逐漸下降，致癇后24 h兩組大鼠腎組織ERK1/2表達均回到0 h水平（Pgt;0.05），對致癇組及坎地沙坦干預兩組大鼠腎組織ERK1/2蛋白表達進行組間比較結果顯示，坎地沙坦組2 h（致癇組：20 229.18±2 067.27，坎地沙坦組：16 878.19±2 693.97，Plt;0.01）、6 h（致癇組：39 217.34±4 443.33，坎地沙坦組：31 924.85±4 383.80，Plt;0.01）、12 h（致癇組：16 610.11±2 953.03，坎地沙坦組：13 393.16±2 269.42， Plt;0.05）ERK1/2表達降低。 結論 ERK1/2在KA致癇大鼠腎組織中表現為短時程表達增加，坎地沙坦可使腎組織ERK1/2表達降低。【Abstract】 Objective To study the effect of candesartan on extracellular signal-regulated kinase (ERK) 1/2 protein expression of renal cells in epilepsy rats induced by kainic acid (KA) and its mechanism. Methods A total of 105 male Wistar rats were randomly divided into three groups: control group (A1-5, n=35), epilepsy group (B1-5, n=35), and candesartan group (C1-5, n=35). The sign 1-5 meant respectively 0, 2, 6, 12, and 24 hours after epilepsy. Epilepsy rat models were made by injecting KA into amygdala under three-dimensional positioning devices. Lavage fixation, paraffin embedding of the renal tissue, and immunohistological test were carried out at different time points after epilepsy was induced, and ERK1/2 protein expression level was tested. Results Compared with the control group, the protein expression of ERK1/2 increased significantly 2 hours after epilepsy in groups B and C (ERK1/2 level 2 hours after epilepsy, group B: 20 229.18±2 067.27, group C: 16 878.19±2 693.97 vs. group A: 8 054.24±975.90, P＜0.01), and both attained its peak 6 hours after epilepsy (ERK1/2 level 6 hours after epilepsy, group B: 39 217.34±4 443.33, group C: 31 924.85±4 383.80 vs. group A: 8 575.24±1 040.82, P＜0.01), and then decreased gradually to the level immediately after epilepsy 24 hours later. There were significant differences in the level of ERK1/2 protein expression between group B and C 2, 6, and 12 hours after epilepsy was induced (2 hours, group B: 20 229.18±2 067.27 vs. group C: 16 878.19±2 693.97, P＜0.01; 6 hours, group B: 39 217.34±4 443.33 vs. group C: 31 924.85±4 383.80, P＜0.01; 12 hours, group B: 16 610.11±2 953.03 vs. group C: 13 393.16±2 269.42, P＜0.05). Conclusions The Extracellular signal-regulated kinase1/2 protein expression of renal tissue in epilepsy rats induced by KA increases shortly after epilepsy. Candesartan can decrease the protein expression of ERK1/2 in the renal tissue of epilepsy rats.
Objective To evaluate the efficacy of statins pretreatment in patients before percutaneous coronary intervention (PCI). Methods Published literature on relevant randomized controlled trials (RCTs) were retrieved via electronic and handsearch in databases CNKI, CBM, MEDLINE and The Cochrane Library from January 1990 to May 2011. The references of these articles were also retrieved. Two reviewers independently identified articles according to the inclusion and exclusion criteria, extracted the data, assess the quality of the included studies, and then conducted meta-analysis using RevMan 5.0 software. Results A total of 10 trials involving 3 012 patients were included. The results of meta-analyses showed that: during the periprocedural period, the trial group had a lower incidence than the control group (98 of 1 514 cases, incidence 6.5%) in periprocedural myocardial infarction with a significant difference (OR=0.43, 95% CI 0.34 to 0.56, Plt;0.000 01). The composite of death, myocardial infarction, or target vessel revascularization in one month, essentially driven by periprocedural myocardial infarction, was reported 6.8% in the trial group and 15.1% in the control group (OR=0.41, 95% CI 0.32 to 0.53, Plt;0.000 01). Conclusion Current evidence supports the effectiveness of statin pretreatment used to reducing the rate of periprocedural myocardial infarction in patients before receiving PCI.