纳洛酮是一种非选择性阿片受体拮抗剂，主要用于急性阿片类药物过量或中毒的管理。先前研究显示，纳洛酮具有抗炎和抗氧化性质。Concanavalin A（Con A）模型是一种常见且基础确立的自身免疫性肝炎动物模型，与人体发生的病理变化非常相似。本研究证明，纳洛酮低剂量（LD NX）能够改善肝功能，减轻Con A诱导的肝损伤，表现为清晰降低血清氨基转移酶、胆红素的浓度，并增强白蛋白的产生，以及肝脏病理变化的改善。此外，共刺激物肿瘤坏死因子-α（TNF-α）、γ干扰素（IFN-γ）、白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）在LD NX预处理的动物中被高度抑制，通过干扰TLR4/NF-κB以及JNK信号通路。进一步，LD NX预处理的动物中氧化应激被明显减轻，表现为肝组织内丙二醛的大幅下降、Nrf2、HO-1表达的增加，以及内源抗氧化剂超氧化物歧化酶、过氧化氢酶和谷胱甘肽的产生。总之，本研究证明，LD NX通过调节炎症细胞因子的分泌和干扰氧自由基的产生，具有缓解Con A诱导的自身免疫性肝炎的能力。© 2023. 作者。

Naloxone is a non-selective opiate receptor antagonist that is mainly used in the management of acute opioid overdose or intoxication. Previously, naloxone has been shown to have anti-inflammatory and antioxidant properties. Concanavalin A (Con A) model is a common and well established animal model of autoimmune hepatitis that closely resembles the pathological alterations that occur in human. The present study demonstrates that a low dose of naloxone (LD NX) has the ability to improve hepatic function and attenuate hepatic damage induced by Con A as indicated by a clear reduction in serum aminotransferase, bilirubin and enhancement of albumin production as well as liver pathological changes. Also, The proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interferon- γ (IFN-γ), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were highly suppressed in animals pretreated with LD NX via interference with TLR4/NF-κB as well as JNK signaling pathways. Furthermore, oxidative stress was highly attenuated in animals pretreated with LD NX as indicated by high reduction in hepatic MDA and an increase in Nrf2, HO-1 expression and subsequent production of the endogenous antioxidants, SOD, CAT and GSH. Collectively, this study demonstrates that LD NX has the ability to mitigate Con A-induced autoimmune hepatitis via modulation of inflammatory cytokines secretion and interference with reactive oxygen species generation.© 2023. The Author(s).