Xiao Min, Liu Chong-Bin, Sun Wei, Dong Miao-Wu, Hu Guo-Xin, Li Jun-Wei
Laboratory Animal Center, Wenzhou Medical College, Wenzhou 325035, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Jan;28(1):84-8.
To examine dietary zinc supplementation could alleviate the damage of alcoholic liver disease and the relationship with the expression of hepatocyte nuclear factor 4alpha (HNF-4alpha).
40 adult C57 BL/6 mice were randomly divided into four groups (n = 10): control, zinc, ethanol and zinc plus ethanol, which were sacrificed after fed four different diets for 6 months. Zinc sulfate was added in the drinking water of the Zinc and Zinc Plus Ethanol group and the content was 75 mg/L. Liver regeneration was assessed by immunohistochemical staining of proliferating cell nuclear antigen (PCNA), and the expression of HNF-4alpha was determined by RT-PCR and Western blot. And as to assess the status of oxidative stress of the mice, malondialdehyde (MDA) and superoxide dismutase (SOD) were detected.
Compared with the control group, the expression level of HNF-4alpha decreased significantly in the ethanol group (P < 0.05), and the content of MDA increased significantly in this group, while the content of SOD declined significantly (P < 0.05). Compared with the ethanol group, the number of PCNA-positive hepatocytes increased significantly, and the expression level of HNF-4alpha also increased in the zinc plus ethanol group (P < 0.05), and the content of SOD increased in this group, while MDA decreased significantly (P < 0.05).
Long term ethanol exposure can lead to oxidoreduction imbalances which can be reversed by zinc supplementation. We suppose that zinc-enhanced liver regeneration is associated with an increase in HNF-4alpha, suggesting that dietary zinc supplementation may have beneficial effects in alcoholic liver disease.
研究膳食补充锌是否能减轻酒精性肝病的损伤及其与肝细胞核因子4α(HNF-4α)表达的关系。
将40只成年C57 BL/6小鼠随机分为四组(n = 10):对照组、补锌组、乙醇组和补锌加乙醇组,给予四种不同饮食6个月后处死。补锌组和补锌加乙醇组的饮用水中添加硫酸锌,含量为75 mg/L。通过增殖细胞核抗原(PCNA)免疫组化染色评估肝再生情况,采用RT-PCR和Western blot检测HNF-4α的表达。同时检测丙二醛(MDA)和超氧化物歧化酶(SOD)以评估小鼠氧化应激状态。
与对照组相比,乙醇组HNF-4α表达水平显著降低(P < 0.05),该组MDA含量显著增加,而SOD含量显著下降(P < 0.05)。与乙醇组相比,补锌加乙醇组PCNA阳性肝细胞数量显著增加,HNF-4α表达水平也升高(P < 0.05),该组SOD含量增加,而MDA显著降低(P < 0.05)。
长期乙醇暴露可导致氧化还原失衡,补锌可逆转这种失衡。我们推测锌增强肝再生与HNF-4α增加有关,提示膳食补锌可能对酒精性肝病有有益作用。