摘要
目的研究四氯化碳(CC l4)所致肝纤维化大鼠肝组织中白介素-1β(IL-1β)及白介素-1β受体(IL-1βR)的表达,探讨肝纤维化的发病机理。方法CC l4所致2、4、6、8周肝纤维化模型及对照组大鼠肝苏木素-伊红染色、免疫组织化学反应,观察肝组织病理变化和IL-1β及IL-1βR的表达。结果对照组大鼠肝组织中IL-1β及IL-1βR无明显表达;2周模型组病理变化以炎症及肝细胞变性为主,肝组织细胞IL-1β及IL-1βR表达较对照组明显增强(P<0.01);4周模型组间质成分增生明显,坏死肝细胞中IL-1β及IL-1βR无明显表达,与2周模型组相比IL-1β及IL-1βR表达减少(P<0.01);6周模型组肝细胞大量坏死,中央静脉及汇管区纤维隔形成,与4周模型组相比IL-1β及IL-1βR阳性细胞明显减少(P<0.01);8周模型组肝组织形成完整的假小叶,肝组织细胞IL-1β及IL-1βR表达程度与6周模型组相似。结论肝纤维化发生、发展的不同阶段,损伤因子均能刺激肝组织细胞表达IL-1β及IL-1βR。
Objective To study the expressions of imerleukin-1β （IL-1β） and interleukin-1β receptors （IL-1β） of liver tissue in rats with hepatic fibrosis induced by CCl4. Method The model of hepatic fibrosis model was established by administration of CCl4 two times a week for 2, 4, 6, 8 weeks respectively. The liver tissues of rats in all groups （including the control group） were stained by hematoxyhn-eosin （HE） and the pathological changes and the expressions of IL-1β and IL - 1βR in rat liver tissues were observed with immunohistochemical response. Results The expressions of IL-1β and IL-1βR in the control group was not significant. In 2 week group the pathological changes were mainly inflammation and hepatocyte degeneration, the expressions of IL-1β and IL-1βR were significantly increased （P 〈 0.01 ） compared with that of the control group. In 4 week group there was a significant proliferation of interstitial substance and the expressions of IL-lo and IL-10R were not obvious in necrosis hepatocytes and decreased compared with that of 2 week group （P 〈0.01 ）. In 6 week group the necrosis of hepatocytes was serious and the fibrotic septa formed around central vein and portal area. The positive cells of IL-1β and IL-1βR decreased obviously compared with that of 4 week group （P 〈 0.01 ）. In 8 week group the pseu-lobules formed in liver tissue and the expressions of IL-1β and IL-1βR were similar to that of 6 week group. Conclusion In the different development phases of hepatic fibrosis the injury factors could stimulate the expressions of IL-1β and IL-1βR in liver cells.
出处
《北京中医药大学学报》
CAS
CSCD
北大核心
2006年第2期98-100,i0001,共4页
Journal of Beijing University of Traditional Chinese Medicine
基金
国家自然科学基金资助项目(No.30130220)
中国人民武装警察部队科研基金资助项目
长江学者和创新团队发展计划资助项目(No.T0413)
