摘要
目的 研究抗独特型抗体 NP30诱导虫卵肉芽肿细胞凋亡的分子机制。方法 BAL B/c小鼠随机分为两组 ,实验组腹腔注射 NP30 10μg/次 ,连续 3次 ,对照组腹腔注射生理盐水 ,分别在尾蚴攻击感染后第 39、4 9、6 4、10 8、112天处死 ,应用免疫组化 S- P法检测凋亡相关基因 Bax、Bcl- 2、Fas、Fas L和 c- Fos的表达 ,原位分子杂交检测 Bax与 Fas m RNA。结果 虫卵肉芽肿细胞均表达Bax、Fas、Fas L和 c- Fos蛋白 ,其中实验组 Bax和 Fas L蛋白表达均高于对照组 (P<0 .0 5 ) ;实验组Fas和 c- Fos蛋白表达在第 6 4天和第 112天低于对照组 ,其余各时间点均高于对照组 (P<0 .0 5 ) ;Bcl- 2蛋白在实验组和对照组均无表达。实验组 Bax和 fas m RNA表达均高于对照组。结论 死亡受体 Fas和 Fas L途径启动了 NP30诱导肉芽肿细胞凋亡的信号 ,NP30通过凋亡相关基因 Bax和
Objective To study the molecular mechanism of apoptosis of cells in egg granuloma induced by anti-idiotypic antibody NP30 of Schistosoma japonicum.Methods BALB/c mice were randomly divided into two groups. The mice of the experimental group were immunized by injecting NP30 intraperitoneally for three times, while the mice of control group were injected normal saline intraperitoneally. The mice were sacrificed respectively on the 39th, 49th, 64th, 108th, 112nd day after challenge with schistosome cercariae. The expressions of apoptosis-related gene Bax, Bcl-2, death receptor Fas, FasL (Fas ligand) and c-Fos were examined by the S-P method of immunohistochemistry,and Bax, mRNA and Fas mRNA investigated by the in-situ hybridization. Results The expressions of Bax, Fas, FasL and c-Fos were positive in granuloma cells of both groups. The expressions of Bax and FasL in experimental group were higher than those in control group (P<0.05). The expressions of Fas and c-Fos in experimental group were higher than those in control group, except lower in the 64th and 112nd. Bcl-2 protein was negative in both experimental and control group. The expressions of Bax mRNA and Fas mRNA in experimental group were higher than those in control group. Conclusions Death receptor Fas and FasL were involved in initiating process of apoptosis of egg granuloma cells induced by NP30, and NP30 could induce the apoptosis of egg granuloma cells by the pathway of expressions of apoptosis-related gene Bax and c-Fos.
出处
《中国血吸虫病防治杂志》
CAS
CSCD
2004年第3期174-177,F004,共5页
Chinese Journal of Schistosomiasis Control
基金
南京医科大学科技发展基金资助项目 ( No.5 45 940 0 )
