Hyperin attenuates inflammation by activating PPAR-γ in mice with acute liver injury (ALI) and LPS-induced RAW264.7 cells

炎症 p38丝裂原活化蛋白激酶 脂多糖 基因沉默 药理学 肿瘤坏死因子α 体内 MAPK/ERK通路 小干扰RNA 过氧化物酶体增殖物激活受体 体外 化学 生物 受体 信号转导 免疫学 生物化学 转染 基因 生物技术
作者
Cheng Huang,Yang Yang,Wanxia Li,Xiaoqin Wu,Xiaofeng Li,Taotao Ma,Lei Zhang,Xiao‐Ming Meng,Jun Li
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:29 (2): 440-447 被引量:44
标识
DOI:10.1016/j.intimp.2015.10.017
摘要

Hyperin (HP) is a flavonoid compound found in various plants like Ericaceae, Guttifera and Celastraceae. The present study has revealed that HP has a variety of pharmacological effects including anti-oxidant, anticancer, and anti-coagulant, especially anti-inflammatory. However, the potential molecular mechanism of anti-inflammatory is still unrevealed. In this study, HP not only significantly attenuated inflammation in C57BL/6J mice with acute liver injury (ALI), but also reduced the expression of TNF-α and IL-6 in lipopolysaccharide (LPS)-induced RAW264.7 cells. Furthermore, our findings showed that HP remarkably induced the expression of PPAR-γ in vivo and in vitro. Interestingly, compared with the HP treatment group, a specific blocking agent of PPAR-γ T0070907 and PPAR-γ small interfering (si)-RNA-mediated silencing in RAW264.7 cells were used to evaluate the involvement of HP in alleviating LPS-induced inflammation. More importantly, over-expression of PPAR-γ had an opposite effect on the expression of TNF-α and IL-6 in LPS-induced RAW264.7 cells after treatment with HP. In addition, HP remarkably inhibited the expression of P-ERK1/2 and P-P38 MAPK. Taken together, all the above results indicate that HP may serve as an effective modulator of PPAR-γ, further down-regulating ERK1/2 and p38 MAPK during the pathogenesis of inflammation.
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