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目的探讨灵芝三萜类化合物联合外源性神经节苷脂(GM1)对癫痫脑损伤早期神经保护作用的效果及机制。方法Sprague-Dawley大鼠随机分为空白对照组、癫痫模型组、灵芝三萜化合物组、溶媒对照组、GM1组、GM1联合灵芝三萜化合物组,除空白对照组外其余各组用戊四氮亚惊厥剂量腹腔注射,复制慢性癫痫模型。双抗体夹心ELISA检测血清和脑脊液中S蛋白-β(S-100β)、C反应蛋白(CRP)及降钙素基因相关肽(CGRP)蛋白含量,放射免疫法检测神经元特异性烯醇化酶(NSE)蛋白含量。结果分别应用灵芝三萜化合物和GM1干预后,大鼠脑脊液和血清S-100β、NSE、CRP蛋白含量与癫痫模型组相比明显降低(P<0.05)、CGRP含量升高(P<0.05),而联合应用两种药物治疗后,大鼠癫痫发作潜伏期明显延长(P<0.05),S-100β、NSE、CRP蛋白含量降低与CGRP含量升高较单一用药效果更明显(P<0.05)。结论灵芝三萜化合物或GM1治疗均可不同程度减轻癫痫脑损伤,而2种药物联合应用对其脑损伤的改善作用更明显,其作用机制可能为通过影响反映脑组织损伤和炎症反应的S-100β、NSE、CRP及CGRP蛋白表达而起到脑神经元保护作用。
Objective To investigate the effect and mechanism of Ganoderma lucidum triterpenoids combined with exogenous ganglioside (GM1) on early neuroprotective effect of epileptic brain injury. Methods Sprague-Dawley rats were randomly divided into blank control group, epilepsy model group, Ganoderma lucidum triterpene compound group, vehicle control group, GM1 group, GM1 combined with Ganoderma lucidum triterpene compound group, except for the blank control group, Subacute dose of subacute injection, replication of chronic epilepsy model. The levels of S-100β, C-reactive protein (CRP) and CGRP in serum and cerebrospinal fluid (CSF) were detected by double antibody sandwich ELISA. The levels of neuronal specific enolase NSE) protein content. Results The levels of S-100β, NSE and CRP in rat cerebrospinal fluid and serum were significantly decreased (P <0.05) and CGRP levels were significantly increased (P <0.05) compared with those in epilepsy model after intervention of Ganoderma lucidum triterpenoids and GM1, Compared with the single drug treatment, the latency of seizure was prolonged in both groups (P <0.05). The decrease of S-100β, NSE and CRP and the increase of CGRP were more obvious than single drug treatment (P <0.05). Conclusion Ganoderma triterpenoids or GM1 treatment can relieve epilepsy brain injury in varying degrees, and the combined effect of two drugs on brain injury is more obvious, the mechanism may be through the influence of brain tissue damage and inflammatory response of S- 100β, NSE, CRP and CGRP protein expression and play a neuronal protective effect.