Jármay K, Gallai M, Karácsony G, Ozsvár Z, Schaff Z, Lonovics J, Kovalszky I
First Department of Internal Medicine, Albert Szent-Györgyi Medical University, Szeged, Hungary.
J Hepatol. 2000 Jun;32(6):993-1002. doi: 10.1016/s0168-8278(00)80104-x.
BACKGROUND/AIMS: Chronic hepatitis C can lead to cirrhosis and hepatocellular carcinoma. Interferon-alfa therapy may prevent the progression of the disease. The expressions of decorin and alfa-smooth muscle cell actin of the extracellular matrix play a central role in liver fibrosis. We set out to assess the expressions of these proteins in chronic hepatitis C patients, and to evaluate how they can be modified by interferon-alfa therapy.
Twenty chronic hepatitis C patients received interferon-alfa-2b therapy for 6 months (group I) or 12 months (group II). Liver biopsy samples were taken before and after the therapy. The alfa-smooth muscle actin-positive cells were determined with a monoclonal antibody, and decorin expression was detected with a polyclonal antibody. The cells were evaluated with a semiquantitative scoring method. For statistical analysis, non-parametric methods were used.
Before the therapy, alfa-smooth muscle actin-labeled cells and marked decorin expression were present throughout all the acinar zones. Interferon-alfa-2b therapy resulted in significant decreases in both the number of alfa-smooth muscle actin-positive cells and the decorin expression. The alfa-smooth muscle actin-positive cells and decorin expression correlated with the histological activity index (R=0.72, p<0.03, R=0.68, p<0.05).
This study demonstrates that a large number of alfa-smooth muscle actin-positive cells and a marked decorin expression are frequent findings in chronic hepatitis C. Treatment with interferon-alfa-2b for 12 months reduced the number of labeled cells and the decorin expression. The results suggest that interferon-alfa-2b is capable of interfering with fibrogenesis in an early and presumably still reversible phase of chronic hepatitis C.
背景/目的：慢性丙型肝炎可导致肝硬化和肝细胞癌。α-干扰素治疗可能会阻止疾病进展。细胞外基质中核心蛋白聚糖和α-平滑肌肌动蛋白的表达在肝纤维化中起核心作用。我们着手评估这些蛋白在慢性丙型肝炎患者中的表达，并评估α-干扰素治疗如何改变它们。
20例慢性丙型肝炎患者接受α-干扰素-2b治疗6个月（第一组）或12个月（第二组）。在治疗前后采集肝活检样本。用单克隆抗体测定α-平滑肌肌动蛋白阳性细胞，用多克隆抗体检测核心蛋白聚糖表达。用半定量评分法评估细胞。进行统计分析时使用非参数方法。
治疗前，所有腺泡区均存在α-平滑肌肌动蛋白标记细胞和明显的核心蛋白聚糖表达。α-干扰素-2b治疗使α-平滑肌肌动蛋白阳性细胞数量和核心蛋白聚糖表达均显著降低。α-平滑肌肌动蛋白阳性细胞和核心蛋白聚糖表达与组织学活动指数相关（R=0.72，p<0.03，R=0.68，p<0.05）。
本研究表明，大量α-平滑肌肌动蛋白阳性细胞和明显的核心蛋白聚糖表达在慢性丙型肝炎中很常见。用α-干扰素-2b治疗12个月可减少标记细胞数量和核心蛋白聚糖表达。结果表明，α-干扰素-2b能够在慢性丙型肝炎的早期且可能仍可逆的阶段干扰纤维生成。
