Modified citrus pectin stops progression of liver fibrosis by inhibiting galectin-3 and inducing apoptosis of stellate cells

被引:54
作者
Abu-Elsaad, Nashwa M. [1 ]
Elkashef, Wagdi Fawzi [2 ]
机构
[1] Mansoura Univ, Fac Pharm, Dept Pharmacol & Toxicol, Mansoura 35516, Adakahlia, Egypt
[2] Mansoura Univ, Fac Med, Dept Pathol, Mansoura 35516, Egypt
关键词
citrus pectin; liver; galectin-3; fibrosis; apoptosis; antioxidant; LIPID-PEROXIDATION; CANCER CELLS; IN-VIVO; ACTIVATION; PHAGOCYTOSIS; PATHWAYS; ASSAY;
D O I
10.1139/cjpp-2015-0284
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Modified citrus pectin (MCP) is a pH modified form of the dietary soluble citrus peel fiber known as pectin. The current study aims at testing its effect on liver fibrosis progression. Rats were injected with CCl4 (1 mL/kg, 40% v/v, i.p., twice a week for 8 weeks). Concurrently, MCP (400 or 1200 mg/kg) was administered daily in drinking water from the first week in groups I and II (prophylactic model) and in the beginning of week 5 in groups III and IV (therapeutic model). Liver function biomarkers (ATL, AST, and ALP), fibrosis markers (laminin and hyaluronic acid), and antioxidant biomarkers (reduced glutathione (GSH) and superoxide dismutase (SOD)) were measured. Stained liver sections were scored for fibrosis and necroinflammation. Additionally, expression of galectin-3 (Gal-3), alpha-smooth muscle actin (SMA), tissue inhibitor metalloproteinase (TIMP)-1, collagen (Col) 1A1, caspase (Cas)-3, and apoptosis related factor (FAS) were assigned. Modified pectin late administration significantly (p < 0.05) decreased malondialdehyde (MDA), TIMP-1, Col1A1, alpha-SMA, and Gal-3 levels and increased levels of FAS, Cas-3, GSH, and SOD. It also decreased percentage of fibrosis and necroinflammation significantly (p < 0.05). It can be concluded that MCP can attenuate liver fibrosis through an antioxidant effect, inhibition of Gal-3 mediated hepatic stellate cells activation, and induction of apoptosis.
引用
收藏
页码:554 / 562
页数:9
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