Abstract

Context

Taxifolin (TAX) has effective anti-inflammatory, antioxidant and hepatoprotective activities, but its potential mechanism has not been revealed.

Objective

To evaluate the potential protective effect of TAX on acute alcohol-induced liver injury in mice.

Materials and methods

Alcoholic liver injury model was established by oral alcohol in mice, and randomly distributed in five groups (n = 10): Normal group (oral saline only); Alcohol group (concentration of fermented alcohol: 56%, 6 mL/kg); TAX groups, mice were orally administered with alcohol, and then TAX with doses of 20, 40, 80 mg/kg, respectively. Oral administration was conducted for 6 weeks.

Results

TAX treatment illustrated that the level of alanine aminotransferase (ALT) was reduced to 65.90 ± 2.26 U/L and aspartate aminotransferase (AST) to 33.28 ± 5.62 U/L compared with alcohol group (ALT 124.51 ± 4.40 U/L, AST 61.70 ± 4.09 U/L), while superoxide dismutase (SOD) was increased to 49.81 ± 2.39 U/mg and glutathione (GSH) to 8.16 ± 0.44 μmol/g, but MDA was reversed to 2.53 ± 0.24 nmol/mg. Histopathological examination showed TAX treatment alleviated alcohol-induced hepatocyte necrosis and inflammatory infiltration. Meanwhile, Western blot and rt-PCR indicated TAX reduced IL-6 to 2.49 ± 0.25 pg/mL and TNF-α to 1.79 ± 0.20 pg/mL, and inhibiting NF-κB activation in liver. Moreover, TAX reversed alcohol-induced apoptosis by regulating the expression of PI3K/Akt and its downstream apoptotic factors.

Conclusions

The research provides novel evidence of the hepatoprotective effect of TAX on alcohol-induced liver injury, while also providing the possibility for future treatment of alcoholic liver disease.

中文翻译：

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紫杉叶素，一种新型食物，通过调节 NF-κB 介导的炎症和 PI3K/Akt 信号通路减轻小鼠急性酒精性肝损伤

摘要

语境

紫杉叶素 (TAX) 具有有效的抗炎、抗氧化和保肝活性，但其潜在机制尚未阐明。

客观的

评估 TAX 对小鼠急性酒精性肝损伤的潜在保护作用。

材料和方法

通过口服酒精建立小鼠酒精性肝损伤模型，随机分为5组（n  =10）：正常组（仅口服生理盐水）；酒精组（发酵酒精浓度：56%，6 mL/kg）；TAX 组，小鼠口服酒精，​​然后分别以 20、40、80 mg/kg 的剂量给予 TAX。口服给药6周。

结果

TAX 治疗表明，与酒精组（ALT 124.51 ± 4.40 U/L，AST 61.70 4.09 U/L)，而超氧化物歧化酶 (SOD) 增加到 49.81 ± 2.39 U/mg，谷胱甘肽 (GSH) 增加到 8.16 ± 0.44 μmol/g，但 MDA 被逆转到 2.53 ± 0.24 nmol/mg。组织病理学检查显示 TAX 治疗减轻了酒精诱导的肝细胞坏死和炎症浸润。同时，蛋白质印迹和 rt-PCR 表明 TAX 将 IL-6 降低至 2.49 ± 0.25 pg/mL，将 TNF-α 降低至 1.79 ± 0.20 pg/mL，并抑制肝脏中的 NF-κB 活化。此外，TAX 通过调节 PI3K/Akt 及其下游凋亡因子的表达来逆转酒精诱导的细胞凋亡。

结论

该研究为 TAX 对酒精性肝损伤的保肝作用提供了新证据，同时也为未来治疗酒精性肝病提供了可能。