Capsaicin Inhibits Dimethylnitrosamine-Induced Hepatic Fibrosis by Inhibiting the TGF-β1/SmadPathway via Peroxisome Proliferator-Activated Receptor Gamma Activation

被引:74
作者
Choi, Jae Ho [1 ]
Jin, Sun Woo [1 ]
Choi, Chul Yung [2 ]
Kim, Hyung Gyun [1 ,4 ]
Lee, Gi Ho [1 ]
Kim, Yong An [1 ]
Chung, Young Chul [3 ]
Jeong, Hye Gwang [1 ]
机构
[1] Chungnam Natl Univ, Coll Pharm, Daejeon 34134, South Korea
[2] Jeollanamdo Inst Nat Resources Res, Jeollanamdo, South Korea
[3] Int Univ Korea, Dept Food Sci, Jinju, South Korea
[4] Mokpo Marine Food Ind Res Ctr, Dept Res Planning Team, Mokpo, South Korea
基金
新加坡国家研究基金会;
关键词
INDUCED LIVER FIBROSIS; NF-KAPPA-B; STELLATE CELLS; EXTRACELLULAR-MATRIX; CARBON-TETRACHLORIDE; DIETARY CAPSAICIN; OXIDATIVE STRESS; NATURAL-PRODUCTS; PPAR-GAMMA; TNF-ALPHA;
D O I
10.1021/acs.jafc.6b04805
中图分类号
S [农业科学];
学科分类号
082806 [农业信息与电气工程];
摘要
Capsaicin (CPS) exerts many pharmacological effects, but any possible influence On liver fibrosis remains unclear. Therefore, we, evaluated the inhibitory effects of CPS on dimethylnitrosamine (DMN) and TGF-beta 1-induced liver fibrosis in rats and hepatic stellate cells (HSCs). CPS inhibited DMN-induced hepatotoxicity, NF-kB activation, and collagen accumulation. CPS also suppressed the DMN-induced increases in alpha-SMA, collagen type I, MMP-2, and TNF-alpha In addition, CPS inhibited DMN-induced TGF-beta 1 expression (from 2.3 +/- 0.1 to 1.0 +/- 0.1) and Smad2/3 phosphorylation (from 1.5 +/- 0.1 to 1.1 +/- 0.1 and from 1.6 +/- 0.1 to 1.1 +/- 0.1, respectively) by activating Smad7 expression (from 0.1 +/- 0.0 to 0.9 +/- 0.1)via PPAR-y induction (from 0.2 +/- 0:0 to 0.8 +/- 0.0) (p < 0.05). Furthermore, in HSCs, CPS inhibited the TGF-beta 1-induced increases in alpha-SMA and collagen. type I expression, via PPAR-y activation. These results indicate that CPS can ameliorate ]hepatic fibrosis-by inhibiting the TGP-beta 1/Smad pathway via PPAR-y activation.
引用
收藏
页码:317 / 326
页数:10
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