CAJ | 학술논문

目的：：通过比较巨细胞病毒感染新生鼠与正常新生鼠脾脏组织维甲酸相关孤儿核受体γt ( RORγt ）与IL-17的表达水平，为巨细胞病毒感染的发病机制提供实验依据。方法：24只新生BALB／c小鼠出生3 d时腹腔注射MCMV病毒悬液制备MCMV播散性感染模型(即病毒组），分别于造模后第3、7、14天处死8只小鼠，取脾脏组织备用；对照组(24只）腹腔注射等量的无菌生理盐水，同病毒组分为3个时点亚组。应用半定量RT-PCR及Western blot 检测各组脾脏MCMV DNA、RORγt mRNA、IL-17 mRNA及RORγt蛋白的表达情况。结果：病毒组脾脏组织中可见MCMV DNA表达，而对照组没有，病毒组RORγt mRNA、IL-17 mRNA及RORγt蛋白表达随着感染时间的延长，表达逐渐增加，且同时间点表达量均明显高于对照组，差异有统计学意义( P＜0.05）。结论：IL-17与RORγt可诱导巨细胞病毒的炎症反应，参与MCMV的发病机制。
목적：：통과비교거세포병독감염신생서여정상신생서비장조직유갑산상관고인핵수체γt ( RORγt ）여IL-17적표체수평，위거세포병독감염적발병궤제제공실험의거。방법：24지신생BALB／c소서출생3 d시복강주사MCMV병독현액제비MCMV파산성감염모형(즉병독조），분별우조모후제3、7、14천처사8지소서，취비장조직비용；대조조(24지）복강주사등량적무균생리염수，동병독조분위3개시점아조。응용반정량RT-PCR급Western blot 검측각조비장MCMV DNA、RORγt mRNA、IL-17 mRNA급RORγt단백적표체정황。결과：병독조비장조직중가견MCMV DNA표체，이대조조몰유，병독조RORγt mRNA、IL-17 mRNA급RORγt단백표체수착감염시간적연장，표체축점증가，차동시간점표체량균명현고우대조조，차이유통계학의의( P＜0.05）。결론：IL-17여RORγt가유도거세포병독적염증반응，삼여MCMV적발병궤제。
Objective:By comparing the expression levels of retinoic acid-related orphan nuclear receptorγt( RORγt) and in-terleukin-17 ( IL-17 ) in newborn rats′spleen tissue with cytomegalovirus infection with normal newborn to provide experimental evidence for the pathogenesis of CMV infection.Methods:Forty-eight newborn BALB/c mice were randomly divided into control group and MCMV group.Mice in virus group was given intraperitoneal injection of MCMV virus suspension,while the control group were given the same dose of normal saline as controls.Eight mice in the two groups were killed at day 3,7 and 14.The animal were sacrificed at day 3,7 and 14( n=8 for each interval) and spleens were obtained from the two groups.MCMV DNA,RORγt mRNA,IL-17 mRNA and protein of RORγwere detected by using RT-PCR and Western blot between the two groups.Results:Expression of MCMV DNA was in-creased in the MCMV group but absent in the control group.RORγt mRNA, IL-17 mRNA and protein expression of RORγt were significantly higher than the normal control group,with the extension of the infection time gradually increased( P<0.05 ) .Conclusion:The IL-17 and RORγt in spleen tissue may take part in the inflammatory response induced by MCMV, and may be involved in the pathogeneses of MCMV injury.