谷氨酰胺对实验性大鼠畸形腺窝灶的影响及其机理研究

Effect and Mechanism of Glutamine to The Aberrant Crypt Foci in Rats

目的探讨谷氨酰胺对醋酸损伤的大鼠畸形腺窝灶的影响及其机理。方法Wistar大鼠30只均分成对照组、醋酸组和谷氨酰胺组3组。用1%醋酸灌注大鼠结肠制成大鼠结肠损伤模型,谷氨酰胺组在制模后第2d开始给予谷氨酰胺灌胃。各组于制模14d后处死动物,取损伤结肠组织进行HE染色,观察病理组织学变化;对所取的结肠隐窝用盐酸浸润消化法分离,于扫描电镜下观察隐窝情况;用免疫组织化学方法检测结肠黏膜上皮细胞中CD44和细胞间黏附分子-1(intercellul aradhesion molecule-1,ICAM-1)的表达情况。结果制模后14d,醋酸组畸形腺窝灶数目较谷氨酰胺组和对照组多,且呈分叉状。谷氨酰胺组结肠黏膜上皮细胞中ICAM-1和CD44表达阳性细胞数(302.1±30.1、298.6±28.3)均明显高于对照组(223.6±23.5、221.5±28.6)和醋酸组(198.5±19.5、215.3±17.8),P<0.05;而后2组间差异无统计学意义(P>0.05)。结论谷氨酰胺能减少醋酸损伤大鼠畸形腺窝灶的形成;增加CD44和ICAM-1的表达,可能是谷氨酰胺能够减少其形成的一个重要因素。

Objective To explore the effect and mechanism of glutamine to the aberrant crypt foci （ACF） in rat injured by acetic acid. Methods Thirty Wistar rats were averagely divided into three groups： control group, acetic acid group and glutamine group. The colon of the rat was infused with 1% acetic acid. Started to garage with glutamate two days after modeling glutamine group. The injured colons were studied after fourteen days with light and scanning electronic microscope. Paraffin sections of specimens were prepared and stained with HE. The colon crypts were isolated by HC1 digestion method. The expressions of CD44 and ICAM-1 in the epithelial cell of the large intestine mucosa were detected by immunohistochemistry method. Results On the days of 14, the number of ACF in the glutamine group were remarkably decreased as compared with that of the acetic acid group and a branch-like. The expressions of ICAM-1 and CD44 （every 1 000 cells） were 302.1±30.1 and 298.6±28.3 in glutamine group, 223.6±23.5 and 221.5±28. 6 in control group, 198.5±19.5 and 215.3±17.8 in acetic acid group, respectively. While the expressions of CD44 and ICAM-1 in intestine were increased remarkably in the glutamine group compared with the control group and acetic acid group （P〈0.05）. Conclusion Glutamine could decrease the formation of the ACF injured by acetic acid. Increasing the expressions of CD44 and ICAM-1 may be one of the important factors to decrease the ACF.