The aim of this study was to investigate the role of scoparone (SCO) in hepatic fibrosis. For this, we conducted in vivo and in vitro experiments. In vivo rats that were divided into six groups, control, carbon tetrachloride, and colchicine, as well as SCO groups, SCO50, SCO100, and SCO200 treated with 50, 100, and 200 mg/kg SCO doses, respectively. Furthermore, SCO was shown to inhibit Toll‐like receptor‐4 (TLR‐4)/nuclear factor kappa‐B (NF‐κB; TLR‐4/NF‐κB) signals by inhibiting TLR‐4, which in turn downregulates the expression of MyD88, promotes NF‐κB inhibitor‐α, NF‐κB inhibitor‐β, and NF‐κB inhibitor‐ε activation, while inhibiting NF‐κB inhibitor‐ζ. Subsequently, the decrease of phosphorylation of nuclear factor‐κB levels leads to the downregulation of the downstream inflammatory factors' tumor necrosis factor‐alpha (TNF‐α), interleukin‐6 (IL‐6), and IL‐1 beta, thus weakening hepatic fibrosis. Notably, the SCO200 treated group presented the most significant improvement. Hence, we conclude that SCO alleviates hepatic fibrosis by inhibiting TLR‐4/NF‐κB signals.

中文翻译：

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司可波酮通过抑制TLR‐4 / NF‐κB途径减轻肝纤维化

这项研究的目的是调查可可酮（SCO）在肝纤维化中的作用。为此，我们进行了体内和体外实验。分为六组的体内大鼠：对照组，四氯化碳和秋水仙碱，以及SCO组，分别以50、100和200 mg / kg SCO剂量治疗的SCO50，SCO100和SCO200。此外，SCO被证明可通过抑制TLR-4来抑制Toll样受体4（TLR-4）/核因子kappa-B（NF-κB; TLR-4 /NF-κB）信号，从而下调表达。 MyD88的作用可促进NF-κB抑制剂-α，NF-κB抑制剂-β和NF-κB抑制剂-ε活化，同时抑制NF-κB抑制剂-ζ。随后，核因子κB水平的磷酸化降低导致下游炎性因子的肿瘤坏死因子-α（TNF-α）的下调，白介素-6（IL-6）和IL-1 beta，从而减弱了肝纤维化。值得注意的是，经SCO200处理的组表现出最显着的改善。因此，我们得出结论，SCO通过抑制TLR-4 /NF-κB信号减轻了肝纤维化。