摘要
目的研究四氯化碳诱导的实验性大鼠肝纤维化不同阶段体内晚期糖基化终末产物的变化情况, 以及晚期糖基化终末产物抑制剂氨基胍对肝纤维化的干预作用。方法 SD大鼠分为3组：对照组、模型组、氨基胍干预组。检测四氯化碳诱导的大鼠肝纤维化及氨基胍干预后不同阶段血清及肝组织匀浆晚期糖基化终末产物含量,血清透明质酸水平,并对照观察肝脏的组织病理学改变进行肝纤维化程度评分。结果血清及肝组织匀浆晚期糖基化终末产物含量、透明质酸水平以及肝纤维化评分,肝纤维化12周组高于对照组(t值分别为3．26、3．49、4．70和25．4,P值均＜0．01),氨基胍干预组低于肝纤维化组(t值分别为2．11、2．11、 2．93和2．47,P值均＜0．05)。血清及肝组织匀浆晚期糖基化终末产物含量与血清透明质酸水平呈线性相关。结论肝纤维化晚期血清及肝组织匀浆晚期糖基化终末产物含量是增高的。一定程度上,体内晚期糖基化终末产物水平可以反映肝纤维化情况。氨基胍对四氯化碳诱导的实验性大鼠肝纤维化有一定的干预作用。
Objectives To study the changes of advanced glycation end products （AGEs） in different phases of a rat liver fibrosis model induced by CCI4, and the interventional effect of aminoguanidin （AG）. Methods Fifty-four SD rats were divided into three groups： a control group, a CCI4 model group and an intervention group. Their blood serum AGEs and hyaluronic acid （HA） and AGEs in their liver homogenates were measured. These measurements were correla- tively assessed to the degrees of liver fibrosis at different phases of the rat model before and after the intervention with aminoguanidin. Results The content of AGEs in their blood sera and liver homogenates, and the level of blood serum HA, and the score of fiver fibrosis degree at week 12 in our rat liver fibrosis mode groups were significantly higher than those in the control group （P 〈 0.01）. In the intervention group with aminoguanidin, these figures were lower than those in the fiver fibrosis model group （P 〈 0.05）. The content of AGEs in their blood sera and fiver homogenates had a linear correlation with the level of HA in their blood sera. Conclusion The contents of AGEs in their blood sera and liver homogenates were increased in the late phase of our rat liver fibrosis model. To some extent, the level of AGEs may reflect the fibrosis degree of the rat livers. Aminoguanidin has an interventional effect in our CCl4 induced rat liver fibrosis model.
出处
《中华肝脏病杂志》
CAS
CSCD
北大核心
2006年第3期178-182,共5页
Chinese Journal of Hepatology
关键词
肝纤维化
氨基胍
晚期糖基化终末产物
Liver fibrosis
Aminoguanidin
Advanced glycation end products
