Immune hepatic injury is a liver disease closely related to an immune imbalance of T cells and macrophages. Our previous series of studies have demonstrated that taraxasterol isolated from Taraxacum possesses great anti-inflammatory and immunomodulatory effects in vivo and in vitro. In this study, we explored the preventive effects of taraxasterol and its underlying mechanisms on concanavalin A (Con A)-induced acute hepatic injury in mice. It was found that treatment with taraxasterol significantly decreased the Con A-induced increase of liver index, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and hepatic malondialdehyde (MDA) levels, and increased the Con A-induced decrease of hepatic glutathione (GSH) and superoxide dismutase (SOD) production. Taraxasterol also significantly inhibited the release of pro-inflammatory cytokines tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-1β, interferon-γ (IFN-γ) and IL-4. In addition, treatment with taraxasterol alleviated the hepatic histopathological injury and apoptosis induced by Con A. Furthermore, taraxasterol dramatically down-regulated the expressions of T toll-like receptor (TLR2), TLR4 and nuclear factor-κappaB (NF-κB) p65, and decreased the expression ratio of Bax/Bc1-2 in hepatic tissues. These findings suggest that taraxasterol prevents Con A-induced acute hepatic injury in mice by inhibiting TLRs/NF-κB inflammatory signalling pathway and promoting Bax/Bc1-2 anti-apoptotic signalling pathway.

中文翻译：

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蒲公英中的蒲公英甾醇通过调节TLRs /NF-κB和Bax / Bc1-2信号通路来预防刀豆素A诱导的小鼠急性肝损伤。

免疫性肝损伤是一种与T细胞和巨噬细胞的免疫失衡密切相关的肝病。我们以前的一系列研究表明，从蒲公英中分离出的蒲公英甾醇在体内和体外具有强大的抗炎和免疫调节作用。在这项研究中，我们探讨了蒲公英糖醇的预防作用及其潜在机制对伴刀豆球蛋白A（Con A）引起的小鼠急性肝损伤的预防作用。结果发现，用酒石黄醇治疗可显着降低Con A诱导的肝指数，血清丙氨酸氨基转移酶（ALT）和天冬氨酸转氨酶（AST）和肝丙二醛（MDA）水平的升高，并增加Con A诱导的肝谷胱甘肽降低的程度。 （GSH）和超氧化物歧化酶（SOD）的生产。蒲公英醇还显着抑制促炎细胞因子肿瘤坏死因子-α（TNF-α），白介素-6（IL-6），IL-1β，干扰素-γ（IFN-γ）和IL-4的释放。此外，用酒石甾醇治疗可减轻Con A诱导的肝组织病理学损伤和细胞凋亡。此外，酒石甾醇显着下调了T toll样受体（TLR2），TLR4和核因子-κappaB（NF-κB）p65的表达，降低了肝组织中Bax / Bc1-2的表达率。这些发现表明，他沙甾醇可通过抑制TLRs /NF-κB炎性信号通路并促进Bax / Bc1-2抗凋亡信号通路来预防Con A诱导的小鼠急性肝损伤。taraxasterol减轻了Con A诱导的肝组织病理损伤和细胞凋亡。此外，taraxasterol显着下调了T toll样受体（TLR2），TLR4和核因子-κappaB（NF-κB）p65的表达，并降低了肝组织中Bax / Bc1-2的表达比例 这些发现表明，他沙甾醇可通过抑制TLRs /NF-κB炎性信号通路并促进Bax / Bc1-2抗凋亡信号通路来预防Con A诱导的小鼠急性肝损伤。taraxasterol减轻了Con A诱导的肝组织病理损伤和细胞凋亡。此外，taraxasterol显着下调了T toll样受体（TLR2），TLR4和核因子-κappaB（NF-κB）p65的表达，并降低了肝组织中Bax / Bc1-2的表达比例 这些发现表明，他沙甾醇可通过抑制TLRs /NF-κB炎性信号通路并促进Bax / Bc1-2抗凋亡信号通路来预防Con A诱导的小鼠急性肝损伤。