姜黄素对溃疡性结肠炎作用机制的研究进展  

Mechanisms underlying therapeutic effects of curcumin on ulcerative colitis

作　　者：郭琳[1] 李昌平[1] 

机构地区：[1]泸州医学院附属医院消化内科,四川省泸州市646000

出　　处：《世界华人消化杂志》2014年第20期2863-2869,共7页World Chinese Journal of Digestology

摘　　要：姜黄素是从植物姜黄中提取的一种多酚,近年来大量研究证实姜黄素对溃疡性结肠炎(ulcerative colitis,UC)具有治疗作用.姜黄素通过抑制核因子κB(nuclear factor kappa-B,NF-κB)信号通路、丝裂原活化蛋白激酶(mitogenactivated protein kinase,MAPK)、信号转导子和转录激活子(signal transducers and activators of transcription-3,STAT3)、Toll样受体4(Tolllike receptor 4,TLR-4)信号通路等,降低细胞因子如白介素-23(interleukin 23,IL-23)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、干扰素γ等,提高参与炎症、免疫反应调节的过氧化物酶体增殖物激活受体(peroxisome proliferator-activated receptorγ,PPAR-γ),减少环氧化酶-2(cyclooxygenase-2,COX-2)、诱导性一氧化氮合成酶(inducible nitric oxide synthase,iNOS)的表达,使亚硝酸盐回到基础水平,从而对UC起抗炎、抗氧化应激、抗细胞凋亡等作用.姜黄素治疗UC的作用机制十分复杂,目前尚不十分明确,本文就近来来姜黄素对UC的作用机制作一综述.Curcumin is a polyphenol which is extracted from the plant Curcuma longa. Recent studies showed that curcumin has therapeutic effects on ulcerative colitis. The mechanisms underlying such therapeutic effects on ulcerative colitis include anti-inflammatory, anti-oxidative stress, anti-apoptosis and so on. Curcumin can inhibit the nuclear factor-κB（NF-κB） signaling pathway, mitogen-activated protein kinase（MAPK）, signal transducers and activators of transcription-3（STAT3）, and Toll-like receptor 4（TLR4） signaling pathway, reduce cytokines such as interleukin-23（IL-23）, tumor necrosis factor（TNF）-alpha and interferon gamma, enhance the expression of peroxisome proliferator-activated receptor γ involved in inflammation and immune response regulation, and down-regulate the expression of cyclooxygenase-2（COX-2） and inducible nitric oxide synthase（iNOS）, thereby making nitrites returning to basal levels. In this paper, we will review the recent progress in understanding the mechanisms underlying the therapeutic effects of curcumin on ulcerative colitis.

关 键 词：姜黄素 溃疡性结肠炎 作用机制 核因子ΚB 信号转导子和转录激活子 

分 类 号：R285.5[医药卫生—中药学]