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机构地区:[1]广州医学院第三附属医院神经内科,510150
出 处:《临床神经病学杂志》2013年第2期115-117,共3页Journal of Clinical Neurology
基 金:广东省医学科研基金(A2008290)
摘 要:目的探讨癫痫大鼠脑组织缝隙连接蛋白32(Cx32)的表达及缝隙连接阻断剂甘珀酸(CBX)对其的影响。方法 72只SD大鼠随机分为正常对照组、癫痫组、癫痫+CBX组及癫痫+生理盐水(NS)组。癫痫组又分为(癫痫后)1 h、1 d、3 d、7 d亚组,癫痫+CBX组和癫痫+NS组分别分为3 d、7 d亚组。用氯化锂-匹罗卡品腹腔注射制作癫痫大鼠模型。癫痫造模成功后,癫痫+CBX组给予CBX 10 mg/(kg.d)腹腔注射,癫痫+NS组给予等量NS。采用免疫组化染色和实时荧光定量逆转录-PCR分别检测大鼠海马区、皮质区Cx32蛋白及mRNA的表达水平。结果与正常对照组比较,癫痫组、癫痫+NS组各时间点亚组海马区和皮质区Cx32蛋白、mRNA表达水平及癫痫+CBX组3 d亚组海马区Cx32蛋白的表达水平均显著增高(均P<0.05);以癫痫组1 d亚组最高(P<0.05)。与癫痫+NS组比较,癫痫+CBX组3 d亚组皮质区、7 d亚组海马区和皮质区Cx32蛋白及mRNA的表达水平均显著降低(均P<0.05)。结论癫痫大鼠脑组织Cx32的表达增高,CBX干预能明显抑制其表达。Cx32可能参与了癫痫的发生和发展过程。Objective To explore the expression of Connexin(Cx) 32 in brain tissues of epileptic rats and the effect of gap junctional blocker--Carbenoxolone (CBX) on it. Methods Seventy-two SD rats were randomly divided into normal control group, epilepsy group, epilepsy + CBX group and epilepsy + normal saline (NS) group. The epilepsy group was divided into 1 h, 1 d, 3 d and 7 d subgroups ( after epilepsy), the epilepsy + CBX group and epilepsy + NS group were divided into 3 d and 7 d subgroups respectively. Epileptic rat model was induced with lithium chloride-pilocarpine intraperitoneal injection. After epilepsy modeled, the epilepsy + CBX group was intraperitoneal injected with CBX 10 mg/( kg d), and the epilepsy + NS group was injected with same dose of NS. Cx32 protein and mRNA expression in hippocampus and cortex of rats were detected by immunohistochemistry and real time fluorescent quantitative reverse transcriptase-PCR (RT-PCR) respectively. Results Compared with the normal control group, the expression level of Cx32 protein and mRNA in hippocampus and cortex of each time point subgroup in epilepsy group and epilepsy + NS group as well as the expression level of Cx32 mRNA in hippocampus of 3 d subgroup in epilepsy + CBX group were significantly increased ( all P 〈 0. 05 ) ; and the 1 d subgroup was the highest in the epilepsy group ( P 〈 O. 05 ). Compared with the epilepsy + NS group, the expression level of Cx32 protein and mRNA in cortex of 3 d subgroup of epilepsy + CBX group and those in hippocampus and cortex of 7 d subgroup of epilepsy + CBX group were significantly decreased ( all P 〈 O. 05). Conclusions The Cx32 expression of brain tissue in epileptic rats is significantly increased. The intervention of CBX can significantly inhibit its expression. Cx32 may have participated in the generation and maintenance of epilepsy.
分 类 号:R742.1[医药卫生—神经病学与精神病学]
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