Toll like receptor 2 knock-out attenuates carbon tetrachloride (CC14)-induced liver fibrosis by downregulating MAPK and NF-κB signaling pathways
Toll like receptor 2 knock-out attenuates carbon tetrachloride (CC14)-induced liver fibrosis by downregulating MAPK and NF-κB signaling pathways
复制标题
Toll 样受体 2 敲除可通过下调 MAPK 和 NF-kappa B 信号通路来减轻四氯化碳 (CC1(4)) 诱导的肝纤维化。
DOI：
10.1016/j.febslet.2014.04.042
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发表时间：
2014-06-05
期刊：
影响因子：
3.5
通讯作者：
Zhang, Si
中科院分区：
文献类型：
--
作者：
Ji, Lingling;Xue, Ruyi;Zhang, Si
与 Toll 样受体 (TLR) 相关的先天免疫信号传导是参与肝纤维化进展的关键途径。在这项研究中，我们报道了 TLR2 是四氯化碳 (CCl4) 诱导的肝纤维化所必需的。 CCl4处理后，与野生型（WT）小鼠相比，TLR2（-/-）小鼠的肝酶水平降低，胶原蛋白沉积减少，炎症浸润减少，肝星状细胞（HSC）活化受损。此外，与WT小鼠相比，CCl4处理后，TLR2(-/-)小鼠的促纤维化和促炎基因表达下调，氮素激活蛋白激酶(MAPK)和核因子κB(NF-κB)激活受损。总的来说，我们的数据表明 TLR2 缺陷可以预防 CCl4 诱导的肝纤维化。 (C) 2014 年欧洲生化学会联合会。由 Elsevier B.V. 出版。保留所有权利。
Innate immune signaling associated with Toll-like receptors (TLRs) is a key pathway involved in the progression of liver fibrosis. In this study, we reported that TLR2 is required for hepatic fibrogenesis induced by carbon tetrachloride (CCl4). After CCl4 treatment, TLR2(-/-) mice had reduced liver enzyme levels, diminished collagen deposition, decreased inflammatory infiltration and impaired activation of hepatic stellate cells (HSCs) than wild type (WT) mice. Furthermore, after CCl4 treatment, TLR2(-/-) mice demonstrated downregulated expression of profibrotic and proinflammatory genes and impaired nitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-kappa B) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl4-induced liver fibrosis. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.