美洛昔康对Aβ诱导Alzheimer’s disease大鼠脑内炎症损伤的影响

The effect of meloxicam on the inflammatory reaction induced by beta amyloid protein in alzheimer's disease rats

目的:研究美洛昔康对β-淀粉样蛋白(Aβ)诱导的阿尔茨海默病(AD)模型大鼠脑内炎症损伤的保护作用,并探讨其抑制炎症作用的机制。方法:Aβ1-40海马注射建立AD大鼠模型。免疫组化法观察大鼠海马核因子κBp65(NF-κBp65)和星形胶质细胞(AS)胶质纤维酸性蛋白(GFAP)表达变化;Western-blot法测定大鼠皮层组织GFAP的表达;ELISA法检测大鼠皮层组织肿瘤坏死因子-α(TNF-α)水平变化;RT-PCR法检测大鼠海马组织白细胞介素-1β(IL-1β)mRNA的表达情况。结果:美洛昔康能抑制AD大鼠海马NF-κBp65和GFAP的表达;降低大鼠皮层TNF-α的含量;抑制AD大鼠海马IL-1βmRNA的表达。结论:美洛昔康通过减少AD模型大鼠海马、皮层组织GFAP表达,抑制AS的增生,降低NF-κBp65的活性,减少炎症因子TNF-α和IL-1β的水平,减轻脑内炎症反应。

Objective：To investigate the effect and mechanism of meloxicam on the inflammatory reaction induced by beta amyloid protein（AB） in Alzheimer＇s disease（AD） rats.Methods：The rat model was established by microinjection of Aβ1-40 into hippocampus.The expression of NF-κB p65 and glial fibrillary acidic protein（GFAP） in hippocampus were detected by immunohistochemistry.The content of GFAP in cortex was tested by Western-blot.The content of TNF-α in cortex was tested by ELISA.The expression of IL-1β mRNA was tested by RT-PCR.Results：The expression of NF-κB p65,GFAP and TNF-α as well as IL-1β mRNA were decreased by meloxicam.Conclusion：Meloxicam can reduce the proliferation of astrocyte by decreasing the expression of GFAP in AD model rat＇s hippocampus and cortex.And the depression of NF-κB p65 may significantly decrease the expression of TNF-αI and L-1β to lessen the inflammatory reaction in cerebral tissue.