桂皮醛对小胶质细胞激活和COX-2表达的影响  

Effects of trans-Cinnamaldehyde on microglial activation and COX-2 expression

作　　者：张宗奇[1] 付岩[2] 杨拼 赵杨[2] 徐颖[2] 

机构地区：[1]上海中医药大学附属曙光医院脑病科,上海201203 [2]上海中医药大学生理教研室,上海201203

出　　处：《中药药理与临床》2017年第3期34-38,共5页Pharmacology and Clinics of Chinese Materia Medica

基　　金：国家自然科学基金资助项目(81274119);上海市教育委员会科研创新项目(13YZ050)

摘　　要：目的:神经炎症作为阿尔茨海默氏病(Alzheimer's disease,AD)的主要病理机制之一,主要表现为小胶质细胞激活和炎症因子环氧合酶-2(cyclooxygenase-2,COX-2)的过表达,最终导致神经元损伤和记忆障碍。本研究主要探讨反式桂皮醛(transcinnamaldehyde,TCA)对AD神经炎症过程中小胶质细胞激活和COX-2过表达的抑制作用及其机制。方法:利用脂多糖(lipopolysaccharides,LPS)诱导建立AD的细胞和动物神经炎症模型;采用qRT-PCR和Western blot检测小胶质细胞和小鼠皮质COX-2mRNA和蛋白表达,免疫组化方法观察皮质小胶质细胞形态变化。结果:脂多糖激活原代小胶质细胞后COX-2 mRNA和蛋白表达均明显增多,桂皮醛(10μM)通过降低COX-2 mRNA稳定性抑制小胶质细胞COX-2 mRNA和蛋白的过表达;同时桂皮醛(50 mg/kg)对脂多糖诱导神经炎症小鼠的皮质COX-2 mRNA和蛋白过表达也有抑制作用,并对皮质小胶质细胞形态改变有明显的恢复作用。结论:桂皮醛抑制AD神经炎症的小胶质细胞激活可能是通过降低COX-2过表达发挥作用的。Objective： To investigate the inhibitory effect and its mechanism of trans-Cinnamaldehyde （TCA） on microglial activation and overexpression of COX-2 in AD with neuroinflammation. The cell and animal model with ueuroinflammation were established by LPS stimulation. Methods： Expressions of COX-2 mRNA and protein in primary microglia and cortex of mice were determined by qRT-PCR and Western blot. The morphological changes of mieroglia in cortex were observed by immunohistoehemieal method. Results： The results showed that expressions of COX-2 mRNA and protein obviously increased in primary microglia stimulated by LPS. TCA（ 10 txM）pretreated with primary microglia suppressed the overexpression of COX-2 mRNA and protein by destabilizing iNOS mRNA. Meanwhile, TCA（50 mg/kg） also decreased the overexpression of COX-2 mRNA and protein, and recovered the morphological changes in cortex of neuroinflammatory mice induced by LPS. Conclusion： This study demonstrates that TCA maybe suppress microglial activation in AD with neuroinflammation through decreasing the overexpression of COX-2.

关 键 词：桂皮醛 神经炎症 小胶质细胞 COX-2 

分 类 号：R285[医药卫生—中药学]