英红九号红茶水提物通过调控TNF-α/NF-κB信号通路缓解小鼠的急性酒精中毒

Alleviating Acute Alcohol Intoxication in Mice using Yinghong No.9 Black Tea Extracts to Regulate the TNF-α/NF-κB Signaling Pathway

摘要:

该研究探讨了英红九号红茶水提物（Yinghong NO.9 Black Tea Water Extract，YBTE）缓解小鼠急性酒精中毒作用（Acute Alcoholic Intoxication，AAI）及其机制。采用56°白酒稀释液一次性灌胃方法建立小鼠AAI模型，记录翻正反射消失和恢复时间，检测血清中谷丙转氨酶（ALT）、谷草转氨酶（AST）活性以及血清和肝脏中乙醇脱氢酶（ADH）的活性，采用Western blot法测定肝脏中核因子-κΒ（NF-κB）、炎症因子肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）蛋白表达水平。结果表明，不同剂量YBTE均能延长小鼠入睡时间，也能缩短睡眠时间，其中高剂量组小鼠入睡时间延长到40.89 min（p<0.01），睡眠时间缩短为166.18 min（p<0.01）。与模型组相比，YBTE可降低血清中ALT和AST的活性，提高血清和肝脏中ADH的活性，其中高剂量组ALT活性下降到22.89 U/L（p<0.01），AST活性下降到29.58 U/L（p<0.01），血清ADH提高到43.43 IU/mL（p<0.01），肝脏ADH提高到7.37 IU/mL（p<0.01），并能下调肝脏中p-NF-κB p65、TNF-α和IL-1β蛋白表达量。YBTE具有良好的缓解AAI的作用，其作用机制可能是促进酒精代谢和下调TNF-α/NF-κB信号通路。

Abstract:

To study the effects and mechanisms of Yinghong No.9 black tea water-extract (YBTE) for alleviating acute alcohol intoxication (AAI), mice were subjected to one-time intragastric administration of 56° Baijiu (Chinese Liquor) to establish an AAI model. Subsequently, the time required to lose and regain the righting reflex of the mice were recorded. The alanine transaminase (ALT) and glutamic oxaloacetic transaminase (AST) activities in the serum and alcohol dehydrogenase (ADH) activity both in the serum and liver were measured. Moreover, the expression the nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-1 β (IL-1β) proteins in the liver were measured using western blot analyses. The results showed that sleep onset latency increased and sleep duration decreased for mice treated with various doses of YBTE compared with the model group. More specifically, the sleep onset latency for the high-dose YBTE-treated group increased to 40.89 min (p<0.01) and their sleep duration was 166.18 min (p<0.01). Moreover, the serum activities of ALT and AST were significantly lower and the ADH activity in the serum and liver were both significantly higher in the YBTE-treated groups than in the control group. In particular, the ALT and AST activities in the high-dose group decreased to 22.89 U/L (p<0.01) and 29.58 U/L (p<0.01), respectively, and the ADH activity in the serum and liver increased to 43.43 IU/mL (p<0.01) and 7.37 IU/mL (p<0.01), respectively. Furthermore, the expression of p-NF-κB p65, TNF-α, and IL-1β in the liver were significantly down regulated. In conclusion, AAI can be effectively relieved with YBTE by promoting ethanol metabolism and down regulating the TNF-α/NF-κB signaling pathway.