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目的研究PARP抑制剂3-氨基苯甲酰(3-aminobenzamide,3-AB)对脂多糖(lipopolysaccharide,LPS)诱导的帕金森病(Parkinson’s disease,PD)大鼠的作用及机制。方法大鼠随机分三组:对照组,LPS组和LPS+3-AB组。免疫组化法检测黑质内酪氨酸羟化酶(tyrosine hydroxylase,TH)的表达;ELISA法检测IL-6和IL-10的蛋白含量;Western blot法检测ERK1/2,p-ERK1/2,p38MAPK,p-p38MAPK蛋白表达水平的变化。结果 LPS显著降低大鼠黑质内TH阳性细胞数,升高IL-6的表达水平,降低IL-10的表达水平,增加p-p38MAPK/p38MAPK和pERK1/2/ERK1/2的表达。PARP抑制剂3-AB显著增加TH阳性细胞数,降低IL-6的水平,增加IL-10的水平,降低pERK1/2/ERK1/2的表达,而使p-p38MAPK/p38MAPK的表达增加。结论 3-AB的脑保护作用可能与ERK1/2通路有关。
Objective To investigate the effect and mechanism of PARP inhibitor 3-aminobenzamide (3-AB) on Parkinson’s disease (PD) induced by lipopolysaccharide (LPS) in rats. Methods Rats were randomly divided into three groups: control group, LPS group and LPS + 3-AB group. The expression of tyrosine hydroxylase (TH) in the substantia nigra was detected by immunohistochemistry. The protein levels of IL-6 and IL-10 were detected by ELISA. The expressions of ERK1 / 2, p-ERK1 / 2 , p38MAPK, p-p38MAPK protein expression level changes. Results LPS significantly decreased the number of TH positive cells in substantia nigra and increased the expression of IL-6, decreased the expression of IL-10 and increased the expression of p-p38MAPK / p38MAPK and pERK1 / 2 / ERK1 / 2. PARP inhibitor 3-AB significantly increased the number of TH-positive cells, decreased the level of IL-6, increased the level of IL-10 and decreased the expression of pERK1 / 2 / ERK1 / 2, thereby increasing the expression of p-p38MAPK / p38MAPK. Conclusion The brain protective effect of 3-AB may be related to the ERK1 / 2 pathway.