【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.
ObjectiveTo evaluate the effects of combined bisoprolol and candesartan therapy on left ventricular hypertrophy and left heart function in in elderly patients with hypertension.
MethodsFrom July 2011 to August 2012, 117 elderly inpatients or outpatients with hypertension in our hospital were randomly divided into trial group and control group. Patients in the control group received levamlodipine besylate and bisoprolol, and patients in the trial group received candesartan and bisoprolol.
ResultsThere was no statistical difference between the two groups at baseline. Three months later, there was no obvious difference of the blood pressure levels between the two groups (P>0.05). The parameters of left ventricular hypertrophy and left heart function were improved at the end of follow-up in both the two groups, but the parameters of the trial group improved better than the control group (P<0.05).
ConclusionIn the elderly patients with hypertension, the combined bisoprolol and candesartan or levamlodipine besylate and bisoprolol therapy can improve left ventricular hypertrophy and left heart function, and the results are better for the combination of bisoprolol and candesartan.
