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首页> 外文期刊>Human and Experimental Toxicology >L-Theanine prevents carbon tetrachloride-induced liver fibrosis via inhibition of nuclear factor kappa B and down-regulation of transforming growth factor beta and connective tissue growth factor
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L-Theanine prevents carbon tetrachloride-induced liver fibrosis via inhibition of nuclear factor kappa B and down-regulation of transforming growth factor beta and connective tissue growth factor

机译：L-茶氨酸通过抑制核因子κB和下调转化生长因子β和结缔组织生长因子来预防四氯化碳诱导的肝纤维化

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Here we evaluated the ability of L-theanine in preventing experimental hepatic cirrhosis and investigated the roles of nuclear factor-kappa B (NF-kappa B) activation as well as transforming growth factor beta (TGF-beta) and connective tissue growth factor (CTGF) regulation. Experimental hepatic cirrhosis was established by the administration of carbon tetrachloride (CCl4) to rats (0.4 g/kg, intraperitoneally, three times per week, for 8 weeks), and at the same time, adding L-theanine (8.0 mg/kg) to the drinking water. Rats had ad libitum access to water and food throughout the treatment period. CCl4 treatment promoted NF-kappa B activation and increased the expression of both TGF-beta and CTGF. CCl4 increased the serum activities of alanine aminotransferase and gamma-glutamyl transpeptidase and the degree of lipid peroxidation, and it also induced a decrease in the glutathione and glutathione disulfide ratio. L-Theanine prevented increased expression of NF-kappa B and down-regulated the pro inflammatory (interleukin (IL)-1 beta and IL-6) and profibrotic (TGF-beta and CTGF) cytokines. Furthermore, the levels of messenger RNA encoding these proteins decreased in agreement with the expression levels. L-Theanine promoted the expression of the anti-inflammatory cytokine IL-10 and the fibrolytic enzyme metalloproteinase-13. Liver hydroxyproline contents and histopathological analysis demonstrated the anti fibrotic effect of L-theanine. In conclusion, L-theanine prevents CCl4-induced experimental hepatic cirrhosis in rats by blocking the main pro-inflammatory and pro-fibrogenic signals.
机译：在这里，我们评估了L-茶氨酸预防实验性肝硬化的能力，并研究了核因子-κB（NF-κB）活化以及转化生长因子β（TGF-beta）和结缔组织生长因子（CTGF）的作用。 ）法规。实验性肝硬化是通过向大鼠（0.4 g / kg，腹膜内，每周3次，共8周）给药四氯化碳（CCl4）建立的，同时添加L-茶氨酸（8.0 mg / kg）喝水在整个治疗期间，大鼠可自由获得水和食物。 CCl4处理促进NF-κB活化并增加TGF-beta和CTGF的表达。 CCl4增加了丙氨酸转氨酶和γ-谷氨酰转肽酶的血清活性和脂质过氧化程度，并且还导致谷胱甘肽和谷胱甘肽二硫化物比率的降低。 L-茶氨酸可防止NF-κB的表达增加，并下调促炎性（白介素（IL）-1 beta和IL-6）和纤维化（TGF-beta和CTGF）细胞因子。此外，编码这些蛋白质的信使RNA的水平与表达水平一致降低。 L-茶氨酸可促进抗炎细胞因子IL-10和纤溶酶金属蛋白酶13的表达。肝羟脯氨酸含量和组织病理学分析证明了L-茶氨酸具有抗纤维化作用。总之，L-茶氨酸可通过阻断主要的促炎和促纤维化信号来预防CCl4诱导的大鼠实验性肝硬化。

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