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目的探讨坎地沙坦干预后海仁藻酸(kainic acid,KA)致痫大鼠肾脏细胞外信号调节激酶(ERK1/2)的表达及其变化的机制。方法 105只雄性Wistar大鼠随机分为3组:A1-5对照组、B1-5致痫组、C1-5坎地沙坦组,每组各35只,1-5分别表示癫痫后0、2、6、12及24h。采用立体定位仪下杏仁核内注射KA方法制备大鼠癫痫模型,于致痫后不同时程,进行灌流固定、肾脏组织的石蜡包埋、切片及免疫,组织化学染色,检测不同时程肾脏ERK1/2表达的灰度值。结果与对照组相比,致痫组及坎地沙坦组肾组织于致痫后2hERK1/2表达均开始增加(致痫后2hERK1/2,致癫组:20 229.18±2 067.27,坎地沙坦组:16 878.19±2 693.97,对照组:8 054.24±975.90,P<0.01),致痫后6h两组大鼠肾组织ERK1/2的表达均达到高峰(致痫后6hERK1/2,致痫组:39 217.34±4 443.33,坎地沙坦组:31 924.85±4 383.80,对照组:8 575.24±1 040.82,P<0.01),随后逐渐下降,致痫后24h两组大鼠肾组织ERK1/2表达均回到0h水平(P>0.05),对致痫组及坎地沙坦干预两组大鼠肾组织ERK1/2蛋白表达进行组间比较结果显示,坎地沙坦组2h(致痫组:20 229.18±2 067.27,坎地沙坦组:16 878.19±2 693.97,P<0.01)、6h(致痫组:39 217.34±4 443.33,坎地沙坦组:31 924.85±4 383.80,P<0.01)、12h(致痫组:16 610.11±2 953.03,坎地沙坦组:13 393.16±2 269.42,P<0.05)ERK1/2表达降低。结论 ERK1/2在KA致痫大鼠肾组织中表现为短时程表达增加,坎地沙坦可使肾组织ERK1/2表达降低。
Objective To investigate the expression of extracellular signal - regulated kinase (ERK1 / 2) in canine after kanic acid (KA) epileptic seizure induced by candesartan and its mechanism. Methods 105 male Wistar rats were randomly divided into three groups: A1-5 control group, B1-5 epilepsy group and C1-5 candesartan group, 35 rats in each group, 1-5 represent epilepsy 0, 2,6,12 and 24h. The model of epilepsy was made by injecting KA into the amygdala of stereotaxic apparatus. The epilepsy model was established at different time points after epileptic seizure. Peritoneal perfusion, paraffin embedding, immunohistochemistry and immunohistochemistry were used to detect the expression of ERK1 / 2 expression of the gray value. Results Compared with the control group, the expression of ERK1 / 2 in the epileptogenic group and the candesartan group began to increase 2 h after the onset of epilepsy (2 h ERK1 / 2 after epilepsy, induced epilepsy group: 20 229.18 ± 2 067.27, (P <0.01). The expression of ERK1 / 2 in the renal tissue of the two groups reached a peak at 6h after epilepsy (induced by epilepsy at 6hERK1 / 2, epilepsy Group: 39 217.34 ± 4443.33, candesartan 31 924.85 ± 4 383.80, control group 8 575.24 ± 1 040.82, P <0.01), and then decreased gradually, the expression of ERK1 / 2 expression returned to the level of 0h (P> 0.05), the expression of ERK1 / 2 protein in renal tissue of epileptogenic group and candesartan intervention two groups were compared between groups showed that candesartan 2h Group: 20 229.18 ± 2 067.27, candesartan group: 16 878.19 ± 2 693.97, P <0.01), 6h (epileptogenic group 39 217.34 ± 4443.33, candesartan group 31 924.85 ± 4 383.80, P <0.01), 12 h (epileptogenic group: 16 610.11 ± 2 953.03, candesartan group: 13 393.16 ± 2 269.42, P <0.05). Conclusions ERK1 / 2 expression in the KA-induced epilepsy rat renal tissue increased short-term, candesartan can reduce the expression of ERK1 / 2 in the kidney.