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目的:观察槐定碱(sophoridine,SRI)对大鼠海马组织CA1区ERK信号转导通路的影响。方法:成年雄性SD大鼠72只随机分为生理盐水对照组(n=8),槐定碱组(n=32),PD98059+槐定碱组(n=32)。腹腔注射大剂量槐定碱(47.83mg/kg)建立癫痫模型,应用免疫组化法和Western blot法检测各组大鼠致痫后0.5h、1.5h、5.0h、8.0h海马组织CA1区ERK1、ERK2和p-ERK1/2的免疫阳性神经元数量的变化。结果:免疫组化结果显示生理盐水对照组大鼠海马CA1区有少量的ERK1和ERK2表达,p-ERK1/2仅在胞浆内表达弱阳性,槐定碱致痫0.5h后P-ERK1/2表达迅速增强,在神经元的胞核胞浆内都有表达;同时ERK1和ERK2阳性神经元数量明显多于生理盐水对照组(P<0.05),尤以致痫1.5h后该三种蛋白阳性细胞数量达到最高,5.0h时阳性神经元数量回降,8.0h继续回降,但仍高于生理盐水对照组。经PD98059干预后,槐定碱致痫大鼠海马ERK1、ERK2和P-ERK1,2阳性神经元数量明显低于槐定碱组(P<0.05)。Western blot检测显示痫性发作各时间点大鼠海马组织内ERK1、ERK2和p-ERK1/2蛋白表达较生理盐水对照组显著增多(P<0.05),其中1.5h点组的蛋白表达水平高于其他各时间点组。PD98059+槐定碱组与槐定碱组比较三种蛋白含量明显降低(P<0.05)。结论:槐定碱通过ERK信号通路对大鼠海马组织造成痫性损害。
Objective: To observe the effect of sophoridine (SRI) on ERK signal transduction pathway in CA1 region of rat hippocampus. METHODS: Seventy-two male adult SD rats were randomly divided into normal saline control group (n=8), sophordine base group (n=32), and PD98059+ sophordine base group (n=32). The epilepsy model was established by intraperitoneal injection of high-dose sophoridine (47.83 mg/kg). ERK1 in hippocampal CA1 region was detected at 0.5 h, 1.5 h, 5.0 h, and 8.0 h after epilepsy in each group by immunohistochemistry and Western blot. Changes in the number of immunopositive neurons, ERK2, and p-ERK1/2. Results: The results of immunohistochemistry showed that there was a little expression of ERK1 and ERK2 in hippocampal CA1 region in normal saline control rats. p-ERK1/2 was only weakly positive in cytoplasm, and P-ERK1/0.5 hours after somatostatin-induced epilepsy. 2 The expression increased rapidly and was expressed in the nucleus cytoplasm of neurons; meanwhile, the number of ERK1 and ERK2 positive neurons was significantly higher than that of the normal saline control group (P<0.05), especially after 1.5 h of epilepsy. The number of cells reached the highest, the number of positive neurons decreased at 5.0h, and continued to decline at 8.0h, but still higher than the control group of saline. After intervention of PD98059, the number of ERK1, ERK2, and P-ERK1, 2 positive neurons in the hippocampus of somatostatin-induced epileptic rats was significantly lower than that of sophoridine (P<0.05). Western blot analysis showed that the expression of ERK1, ERK2 and p-ERK1/2 protein in rat hippocampus at each time point of epileptic seizures was significantly higher than that in the normal saline control group (P<0.05). The protein expression level of the 1.5-h point group was higher than that of the control group. Other time points. The content of three proteins in PD98059+ sophordine base group and sophordine base group was significantly reduced (P<0.05). Conclusion: Sophoridine caused epileptic damage to rat hippocampus through ERK signaling pathway.