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重组白介素-1受体拮抗剂对实验性肝损伤保护作用的初步研究
引用本文:邓存良,陈国民,余光开. 重组白介素-1受体拮抗剂对实验性肝损伤保护作用的初步研究[J]. 细胞与分子免疫学杂志, 1999, 0(2): 121
作者姓名:邓存良  陈国民  余光开
作者单位:泸州医学院附属医院传染病科!泸州646000(邓存良,余光开),重庆医科大学病毒性肝炎研究所(陈国民,刘林)
摘    要:白介素1(IL1) 是重要的炎症因子之一, 在肝损伤中起着重要的作用。为研究重组IL1 受体拮抗剂rIL1ra) 对四氯化碳(CCI4) 诱导的肝损伤的保护作用,将24 只Wistar 大鼠随机分为5 组:即正常对照组(n = 5) ,造模组(n = 5) ,rIL1ra 高剂量(0 .5 m g/100 g) 组(n = 5) ,中剂量(0 .2 mg/100 g) 组(n = 5) 和低剂量(o .1m g/100 g) 组(n = 4) 。检测处理6 周末血清肝酶学(ALT,AST) 和肝纤维化指标:Ⅲ型前胶原(Pc Ⅲ) 、透明质酸( HA) 和层粘蛋白(LN) 。结果:与造模组相比较,rIL1ra 各剂量组血清ALT 和AST 的水平下降( P < 0 .001 和P < 0 .01) ,但组间无差异;而对于肝纤维化指标,虽然数值有下降趋势,但只有高剂量才具有统计学意义( P < 0 .05) 。表明rIL1ra(0 .5m g/100 g) 可阻断肝细胞的急、慢性损伤,抑制肝纤维化的形成,从而可间接地反映IL1 参与了CCl4 导致肝损伤的发病过程。

关 键 词:肝纤维化  重组白介素1  受体拮抗剂  四氯化碳

The role of recombinant interleukin 1 receptor antagonist(rIL 1ra) in protecting liver from injury induced by carbon tetrachloride in Wastar rats
Deng Cunliang, Chen Guomin, YuGuangkai, Liu Lin. The role of recombinant interleukin 1 receptor antagonist(rIL 1ra) in protecting liver from injury induced by carbon tetrachloride in Wastar rats[J]. Chinese journal of cellular and molecular immunology, 1999, 0(2): 121
Authors:Deng Cunliang   Chen Guomin   YuGuangkai   Liu Lin
Affiliation:Deng Cunliang, Chen Guomin, YuGuangkai, Liu Lin(Departrnent of Infectious Disease, Affiliated Hospitol, Luzhou Medical College, Luzhou646000)
Abstract:To examine the effect of IL 1ra on blocking the development of experimental hepatic injury induced by carbon tetracholride(CCl4), Wistar rats were divided into five groups, namely, control (n=5), CCl4(n=5), CCl4 rIL 1ra [riL 1ra doses: low: 0.1 mg/100 g/d(n=4), median:0.2 mg/100 g/d(n=5) and high: 0.5 mg/100 g/d(n=5)], respectively. For each group, the serum levels of the ALT, AST, procollagen III (PcIII), hylauronic acid(HA) and laminin (LN) were measured. In group treated with CCl4 rIL 1ra, we observed a decreased serum levels of ALT, AST, Pc III, HA and LN as compared with those treated with CCl4 alone and the decline degrees were dose dependent with rIL 1ra in the serum levels of Pc III, HA, LN while the decline level of ALT, AST in serum did not show the relationship mentioned above. The significant difference in the serum level of ALT, AST (P < 0.001 and P < 0.01) was found in all doses of IL 1ra. but the significant difference in the serum level of PcIII, HA, LN was only found in high dose of rIL 1ra. These findings suggested that administration of rIL 1ra may be effective in preventing the developing of experimental hepatic injury and hepatic fibrosis. It suggests that IL 1 is involved in the developing of hepatic damage induced by CCl4.
Keywords:hepatic fibrosis rIL lra CCl4
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