Chi Cheng, Liu Xiao-Ya, Hou Fei, Yu Xiao-Zheng, Li Chun-Yun, Cui Li-Jian, Liu Rui-Xia, Yin Cheng-Hong
Department of Internal Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, 100026, China.
Department of Emergency, Beijing Chao-Yang Hospital (Jingxi Campus), Capital Medical University, Beijing, 100043, China.
BMC Complement Altern Med. 2018 Feb 5;18(1):52. doi: 10.1186/s12906-018-2119-7.
This study was to evaluate the effects of herbal compound 861 (Cpd861) on ski-related novel protein N (SnoN) and transforming growth factor-β1 (TGF-β1) /Smad signaling in rats with bile duct ligation (BDL)-induced hepatic fibrosis, and to explore the mechanisms of Cpd861 on hepatic fibrosis.
Thirty Wistar male rats were randomly divided into three groups: sham operation, BDL, and Cpd861. To induce hepatic fibrosis, BDL and Cpd861 group rats underwent bile duct ligation. Cpd861 at 9 g/kg/d or an equal volume of normal saline was administered intragastrically for 28 days. Liver injury was assessed biochemically and histologically. Protein and mRNA changes for SnoN and TGF-β1/Smad signaling (TGF-β1, Smad2, phosphorylated Smad2 [p-Smad2], phosphorylated Smad3 [p-Smad3], fibronectin, and collagen III) were determined by Western blotting and quantitative real-time PCR.
BDL rats treated with Cpd861 had significantly alleviated hepatic fibrosis compared to BDL rats not receiving Cpd861 treatment. Moreover, Cpd861 decreased the expression of fibrosis-associated proteins fibronectin and collagen III in liver tissue. Cpd861 administration increased the expression of SnoN protein, did not change SnoN mRNA level, and decreased TGF-β1, p-Smad2, and p-Smad3 protein expression compared to BDL without Cpd861 treatment.
Cpd861 attenuates hepatic fibrosis by increasing SnoN protein expression and inhibiting the TGF-β1/Smad signaling pathway.
本研究旨在评估中药复方861（Cpd861）对胆管结扎（BDL）诱导的肝纤维化大鼠中Ski相关新蛋白N（SnoN）和转化生长因子-β1（TGF-β1）/Smad信号通路的影响，并探讨Cpd861抗肝纤维化的作用机制。
30只雄性Wistar大鼠随机分为三组：假手术组、BDL组和Cpd861组。为诱导肝纤维化，BDL组和Cpd861组大鼠行胆管结扎术。Cpd861按9 g/kg/d或等体积生理盐水灌胃给药28天。通过生化和组织学方法评估肝损伤。采用蛋白质印迹法和实时定量PCR法检测SnoN和TGF-β1/Smad信号通路（TGF-β1、Smad2、磷酸化Smad2 [p-Smad2]、磷酸化Smad3 [p-Smad3]、纤连蛋白和III型胶原）的蛋白和mRNA变化。
与未接受Cpd861治疗的BDL大鼠相比，接受Cpd861治疗的BDL大鼠肝纤维化明显减轻。此外，Cpd861降低了肝组织中纤维化相关蛋白纤连蛋白和III型胶原的表达。与未接受Cpd861治疗的BDL大鼠相比，给予Cpd861可增加SnoN蛋白表达，不改变SnoN mRNA水平，并降低TGF-β1、p-Smad2和p-Smad3蛋白表达。
Cpd861通过增加SnoN蛋白表达和抑制TGF-β1/Smad信号通路减轻肝纤维化。
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