Alcohol-induced liver injury is characterized by strong inflammation. Polysaccharides separated from herbs can prevent ethanol-induced liver injury. Dendrobium officinale Kimura et Migo leaves (D. officinale) are a new food resource that contains a certain amount of polysaccharide. However, the hepatoprotective effects and the potential mechanisms of D. officinale polysaccharide (DOP) remain unknown. Thus, this study aimed to assess the hepatoprotective effects and potential mechanism in vivo and in vitro of DOP. Male Sprague-Dawley rats were used to establish alcohol-induced liver injury models through the oral gavage of absolute alcohol (5 mL/kg) after the oral administration of DOP (400 and 100 mg/kg) for 30 days. Hematoxylin-eosin staining was used for the histological assessments of hepatocyte degeneration, and the AST and ALT levels in the serum and liver tissue were measured. The inflammatory markers were evaluated using ELISA and immunohistochemistry. The potential mechanism of DOP in alcohol-induced liver cell (LO2) injury in vitro was further identified. Results showed that DOP clearly decreased the AST in the serum and hepatic tissue, obviously reduced the production of inflammatory cytokines (such as IL-1β, IL-6, and TNF-α), and can successfully inhibit NF-κB phosphorylation in vivo. In vitro experiments indicated that DOP increased the LO2 cell viability; prevented LDH release prominently; reduced the secretion of IL-1β, IL-6, and TNF-α; and reversed the expression of IL-1β, IL-6, TNF-α, caspase 1, NLRP3, p-NF-κB, and TLR4. Overall, DOP can alleviate ethanol-induced acute liver injury via the TLR4/NF-κB signaling pathway.

中文翻译：

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铁皮石斛多糖通过 TLR4/NF-κB 信号通路在体内外保护乙醇诱导的急性肝损伤

酒精性肝损伤的特点是强烈的炎症。从草药中分离的多糖可以预防乙醇引起的肝损伤。铁皮石斛（D. officinale）是一种含有一定量多糖的新型食物资源。然而，药用多糖（DOP）的保肝作用和潜在机制仍然未知。因此，本研究旨在评估 DOP 在体内和体外的保肝作用和潜在机制。雄性Sprague-Dawley大鼠口服DOP（400和100mg/kg）30天后，通过灌胃无水酒精（5mL/kg）建立酒精性肝损伤模型。苏木精-伊红染色用于肝细胞变性的组织学评估，并测定血清和肝组织中的 AST 和 ALT 水平。使用ELISA和免疫组织化学评估炎症标志物。进一步确定了 DOP 在体外酒精性肝细胞 (LO2) 损伤中的潜在机制。结果表明，DOP明显降低了血清和肝组织中的AST，明显减少了炎症细胞因子（如IL-1β、IL-6和TNF-α）的产生，并能成功抑制体内NF-κB磷酸化。体外实验表明，DOP 增加了 LO2 细胞活力；显着阻止 LDH 释放；减少 IL-1β、IL-6 和 TNF-α 的分泌；并逆转 IL-1β、IL-6、TNF-α、caspase 1、NLRP3、p-NF-κB 和 TLR4 的表达。总体而言，DOP 可以通过 TLR4/NF-κB 信号通路减轻乙醇诱导的急性肝损伤。