Curcumin, quercetin and atorvastatin protected against the hepatic fibrosis by activating AMP-activated protein kinase

被引:17
|
作者
Kabirifar, Razieh [1 ]
Ghoreshi, Zohreh-al-Sadat [1 ]
Rezaifar, Alireza [2 ]
Binesh, Fariba [3 ]
Bamdad, Kourosh [4 ]
Moradi, Ali [1 ]
机构
[1] Shahid Sadoughi Univ Med Sci & Hlth Serv, Sch Med, Dept Biochem, Yazd 8915173149, Iran
[2] Zabol Univ Med Sci, Sch Med, Zabol, Zahedan, Iran
[3] Shahid Sadoughi Univ Med Sci, Dept Pathol, Yazd, Iran
[4] Payame Noor Univ, Dept Biol, Fac Sci, Tehran, Iran
关键词
Liver fibrosis; AMPK; ACC; SREBP-1c; FAS; CPT1a; BILE-DUCT LIGATION; OXIDATIVE STRESS; LIVER-INJURY; LIPID-ACCUMULATION; ACID; RATS; EXPRESSION; CHOLESTEROL; INHIBITION; CIRRHOSIS;
D O I
10.1016/j.jff.2017.11.020
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
We examined the effects of curcumin, quercetin, and atorvastatin on the hepatic fibrosis through measurement of the protein levels of phospho-AMP-activated protein kinase (p-AMPK) and phospho-acetyl-CoA carboxylase (p-ACC) and gene expression of lipogenic genes in bile duct ligation (BDL)-induced fibrotic rats. We divided male Wistar rats into 8 groups (n = 8 for each), four of which were sham and the remaining four received BDL operations. Each rat in the sham or BDL groups was administered quercetin (30 mg/kg/day), curcumin (100 mg/kg) or atorvastatin (15 mg/kg) for 4 weeks. We found that curcumin, quercetin, and atorvastatin treatment led to up-regulation of p-AMPK and carnitine palmitoyl transferase (CPT1a). However, they suppressed the BDL-mediated increase in sterol regulatory element-binding protein-1c (SREBP-1c), ACC1, fatty acid synthase (FAS) and beta hydroxy beta methylglutaryl-CoA reductase (HMGCR) gene expression (P<.05). In summary, we found that curcumin, quercetin, and atorvastatin protected against the hepatic fibrosis by reducing hepatic fat accumulation via AMPK up-regulation.
引用
收藏
页码:341 / 348
页数:8
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