(Z)2‐(5‐(4‐methoxybenzylidene)‐2, 4‐dioxothiazolidin‐3‐yl) acetic acid protects rats from CCl4‐induced liver injury

(Z)2‐(5‐(4‐methoxybenzylidene)‐2, 4‐dioxothiazolidin‐3‐yl) acetic acid protects rats from CCl4‐induced liver injury
复制标题

DOI:
10.1111/j.1440-1746.2011.06913.x
复制
发表时间:
2012-05
影响因子:
4.1
通讯作者:
Zhen-ling Wang;Chong-yang Deng;Hao Zheng;Caifei Xie;Xian-huo Wang;You-fu Luo;Zhi-zhi Chen;Ping Cheng;Li-Juan Chen
Zhen-ling Wang;Chong-yang Deng;Hao Zheng;Caifei Xie;Xian-huo Wang;You-fu Luo;Zhi-zhi Chen;Ping Cheng;Li-Juan Chen
中科院分区:
医学3区
文献类型:
--
作者:
Zhen-ling Wang;Chong-yang Deng;Hao Zheng;Caifei Xie;Xian-huo Wang;You-fu Luo;Zhi-zhi Chen;Ping Cheng;Li-Juan Chen

文献摘要

相似文献

背景与目的:(Z)2-(5-(4-甲氧基苯亚甲基)-2,4-二氧代噻唑烷-3-基)乙酸(MDA)是一种醛糖还原酶(AR)抑制剂。最近的研究表明,AR通过影响细胞因子和趋化因子的核因子κB(NF-κB)依赖性表达而参与炎症的发病机制,因此可能成为炎症病理学的新治疗靶点。本研究评价了MDA在保护大鼠肝脏免受CCl 4损伤和肝纤维化中的体内作用及其机制。
Background and Aim: (Z)2‐(5‐(4‐methoxybenzylidene)‐2, 4‐dioxothiazolidin‐3‐yl) acetic acid (MDA) is an aldose reductase (AR) inhibitor. Recent studies suggest that AR contributes to the pathogenesis of inflammation by affecting the nuclear factor κB (NF‐κB)‐dependent expression of cytokines and chemokines and therefore could be a novel therapeutic target for inflammatory pathology. The current study evaluated the in vivo role of MDA in protecting the liver against injury and fibrogenesis caused by CCl4 in rats, and the underlying mechanisms.