酒精性肝硬化中肝脏再生受到抑制：与信号转导和转录激活因子3（STAT3）激活降低相关。
Liver regeneration is suppressed in alcoholic cirrhosis: correlation with decreased STAT3 activation.
作者信息
Horiguchi Norio, Ishac Edward J N, Gao Bin
机构信息
Section on Liver Biology, Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5625 Fishers Lane, Rm 2S-33, Bethesda, MD 20892, USA.
出版信息
Alcohol. 2007 Jun;41(4):271-80. doi: 10.1016/j.alcohol.2007.04.008.
UNLABELLED
Liver regeneration is suppressed in alcoholic patients; however, the underlying mechanisms are not fully understood. We examined liver regeneration and signal transducer and activator of transcription 3 (STAT3) activation (an important signal for liver regeneration) in cirrhotic livers from alcoholics, hepatitis C virus (HCV) infection, and alcoholic plus HCV infection. Liver regeneration and STAT3 activation were determined by immunohistochemistry analysis of Ki67 and STAT3 phosphorylation, respectively, in 20 alcoholic cirrhosis, 13 HCV cirrhosis, 13 alcoholic+HCV cirrhosis. Alcoholic or alcoholic plus HCV cirrhotic livers had significantly lower Ki67+ and phospho-STAT3+ (pSTAT3+) hepatocytes and bile duct cells than HCV cirrhotic livers. The pSTAT3 positive staining did not correlate with liver injury (elevation of serum levels of aspartate transaminase [AST] and alkaline phosphatase [ALP]) but correlated positively with cell proliferation (Ki67 positive staining).
IN CONCLUSION
liver regeneration is suppressed in alcoholic cirrhotic livers, which may be partly due to decreased STAT3 activation.
未标记
酒精性肝病患者的肝脏再生受到抑制；然而，其潜在机制尚未完全明确。我们研究了酒精性肝硬化、丙型肝炎病毒（HCV）感染以及酒精性合并HCV感染患者的肝硬化肝脏中的肝脏再生情况以及信号转导和转录激活因子3（STAT3）激活情况（肝脏再生的重要信号）。通过对20例酒精性肝硬化、13例HCV肝硬化、13例酒精性合并HCV肝硬化患者的肝脏组织进行免疫组化分析，分别检测Ki67和STAT3磷酸化情况，以确定肝脏再生和STAT3激活情况。酒精性或酒精性合并HCV肝硬化肝脏的Ki67+和磷酸化STAT3+（pSTAT3+）肝细胞及胆管细胞明显少于HCV肝硬化肝脏。pSTAT3阳性染色与肝损伤（血清天冬氨酸转氨酶[AST]和碱性磷酸酶[ALP]水平升高）无关，但与细胞增殖（Ki67阳性染色）呈正相关。
结论
酒精性肝硬化肝脏的肝脏再生受到抑制，这可能部分归因于STAT3激活减少。
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