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目的探讨胃舒胶囊对萎缩性胃炎癌前病变的防治效果及作用机制.方法采用甲硝基亚硝基胍(MNNG)、雷尼替丁及饥饱失常的综合方法,造成大鼠萎缩性胃炎癌前病变气虚血瘀病证结合的动物模型.55只大鼠随机分为正常组(n=10),模型组(n=15),维甲酸组(n=15,40mg/(kg·d)ig),胃舒胶囊组(n=15,3g/(kg·d),ig),观察各组大鼠一般情况、胃粘膜肉眼形态及组织病理学的变化.结果模型组大鼠一般情况差,肉眼形态有典型的萎缩性胃炎粘膜相改变,病理检查显示胃粘膜固有腺体减少(28±07),腺体化生(记分,26±05),异型增生(记分,22±09),胃小凹延长(μm,50±14),粘膜肌增厚(μm,54±13),AgNOR颗粒数(个/胞核,50±13)、增殖带细胞数(142±42)显著增多,与模型组比较,胃舒胶囊组(05±04,07±05,03±05;30±4,21±3,18±03,50±12)与维甲酸组(18±06,18±07,12±07;42±40,30±30,28±08,97±35)均有改善,但以胃舒胶囊组为著(P<001~00?
Objective To investigate the preventive and therapeutic effects of Wei Shu capsule on precancerous lesions of atrophic gastritis and its mechanism. Methods An animal model of combination of nitroglycerin (MNNG), ranitidine and impatient hunger syndrome was used to induce the combination of deficiency of Qi and blood stasis syndrome in rats with atrophic gastritis precancerous lesions. 55 rats were randomly divided into normal group (n = 10), model group (n = 15), retinoic acid group (n = 15,40 mg / 3g / (kg · d), ig), the general situation of rats in each group, the gastric mucosal macroscopic morphology and histopathological changes. Results The rats in the model group were generally poor with typical atrophic gastritis mucosa changes in the naked eye. Pathological examination showed that the intrinsic glands of the gastric mucosa were reduced (28 ± 07) and glandular metaplasia (score 26 ± 05), dysplasia (score 22 ± 09), gastric recess (μm ± 50 ± 14), mucosal muscle thickening (μm, 54 ± 13), number of AgNOR particles 50 ± 13), and the number of proliferating zone cells (142 ± 42) increased significantly. Compared with the model group, Wei Shu capsule group (05 ± 04,07 ± 05,03 ± 05; 30 ± 4,21 ± 3,18 ± 03,50 ± 12) and retinoic acid group (18 ± 06, 1 8 ± 07,12 ± 07; 42 ± 40,30 ± 30,28 ± 08,9 7 ± 35) were improved, but with stomach Shu capsule group (P <0 01 ~ 0 0?