黄芩茎叶黄酮对大鼠缺血性记忆障碍和神经炎症的作用

目的探讨黄芩茎叶黄酮(SSF)对大鼠缺血性记忆障碍和神经炎症的作用。方法雌性SD大鼠双侧颈总动脉永久结扎2个月制备慢性脑缺血记忆障碍模型,脑缺血大鼠造模后于手术第35天ig给予SSF 17.5,35和70 mg.kg-1,连续38 d。通过Morris水迷宫检测大鼠学习记忆能力、免疫组化法测定皮质和海马星形胶质细胞中神经胶质原纤维酸性蛋白(GFAP)表达及酶联免疫吸附(ELISA)法测定皮质中白细胞介素-1β(IL-1β),IL-8,IL-10和肿瘤坏死因子α(TNF-α)含量。结果与假手术组相比,脑缺血模型组大鼠的再学习能力和记忆保持能力显著降低,到达平台的潜伏期显著延长(P<0.01),在目标象限的游泳路程显著缩短(P<0.01);皮质和海马内星形胶质细胞GFAP的表达显著增加(P<0.01);皮质中IL-1β,TNF-α和IL-8水平明显增加(P<0.01)I,L-10水平显著降低(P<0.01)。SSF 17.5,35和70 mg.kg-1均能不同程度地改善脑缺血引起大鼠再学习能力和记忆保持能力障碍,明显缩短到达平台的潜伏期(P<0.05),延长大鼠在目标象限的游泳路程(P<0.05);抑制皮质和海马内星形胶质细胞GFAP的表达(P<0.05);明显降低皮质中IL-1β,TNF-α和IL-8含量,提高IL-10的水平。结论 SSF对大鼠脑缺血性记忆障碍和神经炎症具有明显的改善作用,其作用机制可能是抑制星形胶质细胞增生和脑内炎性细胞因子的生成。

Effects of flavonoids from Scutellaria stems and leaves on memory impairment and nerve inflammation in chronic cerebral ischemia rats

OBJECTIVE To explore the effect of flavonoids from Scutellaria baicalensis stems and leaves (SSF) on memory impairment and nerve inflammation in chronic cerebral ischemia rats. METHODS A chronic cerebral ischemia model was established by bilateral carotid artery occulation of 2 months in female SD rats. Functions of learning and memory were detected by Morris water maze, expression of glial fibrillary acidic protein (GFAP) was observed by immunohistochemical method and the levels of IL-1β, TNF-α, IL-8 and IL-10 were determined with ELISA method. RESULTS Compared with sham group, relearning ability and retention ability significantly decreased, GFAP expression significantly increased, IL-1β, TNF-α and IL-8 levels rose noticeably and IL-10 content was notably lowered in cerebral ischemia rats, respectively(P<0.01). However, compared with cerebral ischemia model group, SSF 17.5, 35 and 70 mg·kg^-1 for 38 d could significantly improve the impairment of relearning ability and retention ability, effectively inhibit GFAP expression (P<0.05), lowered IL-1β, TNF-α and IL-8 levels and enhance IL-10 content (P<0.01). CONCLUSION SSF can reduce memory impairment and nerve inflammation in chronic cerebral ischemia rats, which may be due to the inhibition of the proliferation of astrocyte and lowered inflammatory cytokine production in the brain.