双环醇对实验性脑梗死大鼠脑保护作用及机制

Neuroprotective effect of bicyclol in experimental rat ischemia stroke

目的观察双环醇对大鼠缺血性脑组织中PPAR-γ和NF-κB表达的影响,探讨其脑保护作用及可能的机制。方法采用成年健康雄性Sprague-Dawley大鼠,随机分为假手术组,溶剂对照组,双环醇小剂量组和大剂量组。应用改良Longa线栓法建立大鼠右侧MCAO模型。术后24 h对大鼠进行神经功能评分,用TTC染色法测定脑梗死体积,干湿重法测定脑组织含水量,Western blot法、实时荧光定量PCR法测定PPAR-γ和NF-κB在脑组织中的表达。结果与Vehicle组相比,双环醇大剂量组神经功能评分有所改善,病变侧脑组织含水量减少,脑梗死体积减小(P<0.05);PPAR-γ蛋白和基因表达明显上调,而NF-κB蛋白和基因表达明显下降(P<0.05)。结论在脑缺血的损伤过程中PPAR-γ表达下降而NF-κB表达上调,给予双环醇干预后可以有效减轻脑损伤。其作用可能与上调PPAR-γ,下调NF-κB,减轻炎症损伤有关。

Objective To investigate the potential role of bicyclot in cerebral ischemia and the underlying mechanisms. Methods Male Sprague-Dawley rats were randomly assigned to four groups：Vehicle （pMCAO ＋ 0. 5% sodium carboxymethylcellulose） ,By-L （Vehicle ＋ bicyclol 50 mg/kg）, By-H （Vehicle ＋ bicyclol 100 mg/kg） and Sham. Rat brain ischemia was induced by pMCAO. Neurological deficit, infarct volume, and brain edema were measured at 24 h after stroke. Western blot and real-time quantitative PCR were used to detect the expression of PPAR-γ, and NF-KB. Results Compared with Vehicle group, bicyclol significantly ameliorated neurological deficit, decreased infarct volume and edema, and up-regulated the expression of PPAR-γ （P 〈 0. 05）. Meanwhile, the expression of NF-κB was decreased （P 〈 0. 05）. Conclusion Bicyclol has neuroprotective effect on cerebral ischemia, and this protection may be through up-regulating PPAR-γ/and down-regulating NF-KB expression.