中文摘要：

目的探讨芒果苷对脂多糖（LPS）诱导慢性炎症大鼠模型中MAPK通路的调控作用及其对血清细胞因子表达谱的影响。方法以间断尾iv小剂量LPS（200μg／kg）制备慢性炎症大鼠模型。模型大鼠随机分为模型组，泼尼松（5mg／kg）组与芒果苷高、中、低剂量（200、100、50mg／kg）组，每天ig给药1次，共给药4周。第4周给药末，分别以RT-PCR、蛋白免疫印迹法检测白细胞MAPK通路p38、ERK、JNK基因表达与蛋白磷酸化水平，以抗体微阵列蛋白质芯片检测血清细胞因子表达谱。结果与模型组比较，芒果苷高剂量组白细胞ERK、JNK基因表达以及ERK蛋白磷酸化受到明显抑制，血清细胞间黏附分子1（ICAM-1）、单核细胞趋化蛋白1（MCP-1）、中性粒细胞趋化因子1（INC-1）与血小板源性生长因子（PDGF）水平显著降低。结论芒果苷通过调控白细胞MAPK通路ERK、JNK基因表达以及ERK蛋白磷酸化，降低血清趋化细胞因子水平，从而发挥抗LPS诱导的慢性炎症作用。

英文摘要：

Objective To investigate the regulation of mangiferin on mitogen-activated protein kinases （MAPK） pathway and the serum cytokines expression patterns in chronic lipopolysaceharide （LPS）-induced chronic inflammation of rats. Methods The rat model with chronic inflammation was established by iv low dose （200 μg/kg） intermittent LPS injection via the caudal vein. Rats were randomly divided into model, Prednisone （PNS, 5 mg/kg）, and mangiferin high-, mid-, low-dose （200, 100, and 50 mg/kg） groups. The rats were ig administered with the predetermined drugs once a day within four weeks. At the end of the 4th week, the RT-PCR was applied to evaluate the gene expression of p38, ERK, and JNK in the MAPK pathway, while the Western blotting was executed to detect their protein phosphorylation levels. The protein antibody microarray chip was employed for serum cytokine expression pattern measurement. Results Compared with the model group, both of the expression ofERK, JNK, and the protein phosphorylation of ERK were markedly inhibited in mangiferin high-dose group. The levels of intercellular adhesion molecule 1 （ICAM-1）, monocyte chemoattractant protein 1 （MCP-1）, cytokine-induced neutrophil chemoattractant 1 （INC-1）, and platelet-derived growth factor （PDGF） were significantly lowered. Conclusion Mangiferin could simultaneously regulate the gene expression of ERK, JNK, and the protein phosphorylation of ERK in the MAPK pathway and decrease the serum chemotactic cytokines level.