黄柏抗痛风活性部位筛选及其对腹膜炎小鼠的保护作用

Screen for active anti-gout part of Phellodendri chinensis Cortex and its protective effect on mice with peritonitis

目的 研究黄柏不同萃取部位抗痛风作用,筛选有效部位并初步探究其作用机制。方法 采用单钠尿酸盐(MSU)诱导小鼠腹腔巨噬细胞及骨髓来源巨噬细胞(BMDM)建立细胞痛风模型,经黄柏不同极性部位给药后,ELISA法检测肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)分泌,从而筛选出活性部位,最后研究活性部位在小鼠体内抗痛风作用及相关机制。结果 黄柏醇提液各萃取部位中,正丁醇部位能降低细胞IL-1β水平和巨噬细胞的吞噬能力(P<0.01),但对TNF-α无明显影响(P>0.05)。与模型组比较,正丁醇部位各剂量组小鼠腹腔灌洗液IL-1β、IL-6水平和中性粒细胞募集程度均降低(P<0.05,P<0.01),其中高剂量组效果最明显,但各给药组TNF-α水平无明显变化(P>0.05)。结论 正丁醇部位为黄柏抗痛风活性部位,其抗痛风机制可能是通过降低细胞吞噬MSU晶体的能力,从而减少IL-1β、IL-6等细胞因子释放,进而减少中性粒细胞募集程度,改善痛风症状。

AIM To study the anti-gout effect of different parts of Phellodendri chinensis Cortex, screen for the active fraction and preliminarily explore the mechanism.METHODS The cell models of gout were dosed with different solutions of P. chinensis Cortex following the model establishment upon the mouse peritoneal macrophages and bone marrow derived macrophages(BMDM) by monosodium urate(MSU) induction. Subsequently, the cells had their secretion of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) detected by ELISA for the screening of the active fraction whose anti-gout effect and associated mechanism was studied in mice in vivo.RESULTS Among the extractions of P. chinense Cortex alcohol extract, the n-butanol site was observed with an efficacy in reducing the IL-1β level and the phagocytic ability of macrophages(P<0.01), but without significant effect on TNF-α(P>0.05). Compared with the model group, all the groups dosed with n-butanol part had decreased levels of IL-1β and IL-6 in peritoneal lavage fluid and the recruitment of neutrophils(P<0.05, P<0.01), with the most significant effect found in the high dose group, but no significant change in any of medicated group in term of the TNF-α level(P>0.05).CONCLUSION Being able to improve the gout symptoms, n-butanol fraction of P. chinense Cortex finds its anti-gout activity through suppression of MSU crystal-induced phagocytosis and the associated release of IL-1β, IL-6 and other cytokines, and reduction of neutrophils recruitment.