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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Modified citrus pectin stops progression of liver fibrosis by inhibiting galectin-3 and inducing apoptosis of stellate cells
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Modified citrus pectin stops progression of liver fibrosis by inhibiting galectin-3 and inducing apoptosis of stellate cells

机译：修饰的柑橘果胶通过抑制galectin-3并诱导星状细胞凋亡来阻止肝纤维化进程

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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.
机译：改性柑桔果胶（MCP）是被称为果胶的膳食可溶性柑桔皮纤维的pH调节形式。当前的研究旨在测试其对肝纤维化进展的影响。给大鼠注射CCl4（1 mL / kg，40％v / v，腹腔注射，每周两次，共8周）。同时，从I组和II组的第一周（预防模型）开始，每天在饮用水中施用MCP（400或1200 mg / kg），而在III组和IV组的治疗第5周开始，则每天在饮用水中施用MCP。测量了肝功能生物标志物（ATL，AST和ALP），纤维化标志物（laminin和透明质酸）和抗氧化剂生物标志物（还原型谷胱甘肽（GSH）和超氧化物歧化酶（SOD））。对染色的肝切片进行纤维化和坏死炎症评分。此外，galectin-3（Gal-3），α平滑肌肌动蛋白（SMA），组织抑制剂金属蛋白酶（TIMP）-1，胶原蛋白（Col）1A1，胱天蛋白酶（Cas）-3和凋亡相关因子（FAS）的表达）被分配。改良果胶后期给药显着（p <0.05）降低了丙二醛（MDA），TIMP-1，Col1A1，α-SMA和Gal-3的水平，并增加了FAS，Cas-3，GSH和SOD的水平。它还显着降低了纤维化和坏死性炎症的百分比（p <0.05）。可以得出结论，MCP可以通过抗氧化作用，抑制Gal-3介导的肝星状细胞活化以及诱导凋亡来减轻肝脏纤维化。

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