摘要
目的:探讨健脾化瘀解毒复方"胃痞消"阻断和逆转慢性萎缩性胃炎(CAG)癌前病变的分子机制。方法:采用致癌化合物N-甲基-N′-硝基-N-亚硝基胍(N-methyl-N′-nitro-N-nitrosoguanidine,MNNG)配合饥饱失常和耗气泻下法建立CAG脾虚模型。采用原位末端标记法检测胃黏膜上皮细胞凋亡阳性细胞数,用免疫组化法检测调控蛋白Caspase-3和P53表达阳性细胞数。结果:模型对照胃黏膜细胞凋亡阳性数及Caspase-3和P53的表达均较正常组明显增加(P<0.01);胃痞消3个剂量组(30,20,10 g.kg-1.d-1,qd,ig,给药4周)均能明显降低模型对照组出现的上述变化(P<0.01)。结论:健脾化瘀解毒复方胃痞消治疗CAG的作用机制可能与其下调胃黏膜上皮细胞凋亡调控蛋白Caspase-3和P53的表达,以及抑制黏膜上皮细胞凋亡有关。
Objective : To explore the molecular mechanism of Weipixiao ( WPX), a traditional Chinese medicine compound recipe, with the process method of invigorating the spleen and removing blood stasis and toxic substance(JPHYJD) : It invigorates the spleen and remove blood stasis and toxic substance, on prevention and treating chronic atrophic gastritis(CAG) , to further intervene the occurring of gastric cancer. Methods: The model of CAG rats with syndrome of spleen deficiency was established by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG) and irregular fasting combined with purgative drugs; the influence of WPX on apoptosis, the expression of regulating proteins Caspase-3 and P53 in gastric mucous epithelial cells was observed using TdT-mediated dUTP-biotin nick end labeling( TUNEL) technique and immunohistochemical stain, Results: The apoptosis, the expression of Caspase-3 and P53 in the cells of the model group were fortified than those of normal group(P 〈 0.01 ) ; but decreased in the three dose groups of WPX(P 〈0.01 ). Conclusion : The mechanism of JPHYJD-WPX may be related to down-regulating of the expression of regulating proteins Caspase-3 and P53, and thus decreasing the abnormal activity of apoptosis in the gastric mucous epithelial cells.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2007年第13期1018-1021,共4页
Chinese Journal of New Drugs
基金
广东省自然科学基金项目(04010050)
关键词
健脾化瘀解毒法
胃痞消
慢性萎缩性胃炎
脾虚
细胞凋亡
CASPASE-3
P53
invigorating the spleen and removing blood stasis and toxic substance (JPHYJD)
Weipixiao
chronic atrophic gastritis (CAG)
spleen deficiency
apoptosis
Caspase-3
P53