Effect of ginseng extract on the TGF-β1 signaling pathway in CCl(4)-induced liver fibrosis in rats.
Effect of ginseng extract on the TGF-β1 signaling pathway in CCl(4)-induced liver fibrosis in rats.
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DOI：
10.1186/s12906-016-1507-0
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发表时间：
2017-01-13
影响因子：
--
通讯作者：
Alsharari SD
中科院分区：
文献类型：
--
作者：
Hafez MM;Hamed SS;El-Khadragy MF;Hassan ZK;Al Rejaie SS;Sayed-Ahmed MM;Al-Harbi NO;Al-Hosaini KA;Al-Harbi MM;Alhoshani AR;Al-Shabanah OA;Alsharari SD
肝病是全球主要的健康问题。人参提取物具有抗氧化、免疫调节和抗炎活性。本研究探讨了人参提取物对四氯化碳（CCl 4）诱导的大鼠肝纤维化的影响。雄性Wistar大鼠随机分为4组：对照组、人参组、CCl 4组和CCl 4+人参组。通过腹腔内（I.P）注射3 ml/kg CCl 4（30%橄榄油）每周一次，连续8周诱导肝损伤。对照组腹腔注射橄榄油。编码转化生长因子β（TGF-β）、I型TGF-β受体（TβR-1）、II型TGF-β受体（TβR-II）、母亲抗十项瘫痪同源物2（Smad 2）、Smad 3、Smad 4、基质金属蛋白酶2（MMP 2）、MMP 9、组织抑制剂基质金属蛋白酶-1（TIMP-1）、胶原蛋白1a 2（Col 1a 2）、胶原蛋白3a 1（Col 3a 1）、采用实时荧光定量PCR法检测白细胞介素-8（IL-8）和白细胞介素-10（IL-10）。与CCl 4组相比，人参提取物治疗可减少肝脏脂肪沉积，降低肝脏网状纤维积聚。与对照组相比，CCl 4组肝毒性生物标志物显著增加，编码TGF-β、TβR-I、TβR-II、MMP 2、MMP 9、Smad-2、-3、-4和IL-8的基因表达上调。但与对照组相比，CCl 4处理导致IL-10 mRNA表达显著下调。有趣的是，人参提取物补充完全逆转了肝毒性的生化标志物和CCl 4诱导的基因表达改变。 人参提取物通过调节CCl 4诱导的肝纤维化模型中的TGF-β1/Smad信号通路具有抗纤维化作用。主要目标是抑制TGF-β1、Smad 2和Smad 3的表达。
Liver diseases are major global health problems. Ginseng extract has antioxidant, immune-modulatory and anti-inflammatory activities. This study investigated the effect of ginseng extract on carbon tetrachloride (CCl4)-induced liver fibrosis in rats. Male Wistar rats were divided into four groups: control group, ginseng group, CCl4 group and CCl4 + ginseng group. Liver injury was induced by the intraperitoneal (I.P) injection of 3 ml/kg CCl4 (30% in olive oil) weekly for 8 weeks. The control group was I.P injected with olive oil. The expression of genes encoding transforming growth factor beta (TGF-β), type I TGF-β receptor (TβR-1), type II TGF-β receptor (TβR-II), mothers against decapentaplegic homolog 2 (Smad2), Smad3, Smad4, matrix metalloproteinase 2 (MMP2), MMP9, tissue inhibitor matrix metalloproteinase-1 (TIMP-1), Collagen 1a2 (Col1a2), Collagen 3a1 (Col3a1), interleukin-8 (IL-8) and interleukin -10 (IL-10) were measured by real-time PCR. Treatment with ginseng extract decreased hepatic fat deposition and lowered hepatic reticular fiber accumulation compared with the CCl4 group. The CCl4 group showed a significant increase in hepatotoxicity biomarkers and up-regulation of the expression of genes encoding TGF-β, TβR-I, TβR-II, MMP2, MMP9, Smad-2,-3, -4, and IL-8 compared with the control group. However, CCl4 administration resulted in the significant down-regulation of IL-10 mRNA expression compared with the control group. Interestingly, ginseng extract supplementation completely reversed the biochemical markers of hepatotoxicity and the gene expression alterations induced by CCl4. ginseng extract had an anti‐fibrosis effect via the regulation of the TGF‐β1/Smad signaling pathway in the CCl4‐induced liver fibrosis model. The major target was the inhibition of the expression of TGF‐β1, Smad2, and Smad3.
影响因子：
2.1
作者：
Emzhik M;Rahimi-Moghaddam P;Ebrahimi SA;Keyhanfar F;Moazzam AS
通讯作者：
Moazzam AS