埋线对慢性萎缩性胃炎模型组大鼠胃泌素-17、血管内皮生长因子、肿瘤坏死因子-α表达的影响

Effect of Embedding Thread on Expressions of Gastrin-17,VEGF and TNF-α in Chronic Atrophic Gastritis Model Rats

目的探讨埋线治疗慢性萎缩性胃炎(CAG)的可能机制。方法采用N-甲基-N’-硝基-N-亚硝基胍(MNNG)复制大鼠CAG模型,并将成模大鼠分为埋线组16只和模型组15只,同时预先设立空白组15只;3组均采取蒸馏水结合清洁级普通饲料喂养,埋线组加上埋线治疗,空白组和模型组配合与埋线组大鼠同时间、同强度的抓取和束缚,不进行任何治疗,直至实验疗程结束;疗程结束后,采用酶联免疫吸附(ELISA)测定法检测血浆胃泌素-17(G-17)、血管内皮生长因子(VEGF)、肿瘤坏死因子-α(TNF-α)的含量。结果模型组与埋线组、模型组与空白组大鼠血清G-17、VEGF、TNF-α表达比较差异具有统计学意义(P <0.05);埋线组与空白组大鼠血清G-17、VEGF、TNF-α表达比较差异无统计学意义(P> 0.05);血清G-17表达强度由弱到强的顺序依次为:模型组、埋线组、空白组;血清VEGF、TNF-α表达强度由弱到强的顺序依次为:空白组、埋线组、模型组。结论埋线可能通过调节G-17、VEGF、TNF-α的表达而起到治疗CAG的作用。

Objective To explore the possible mechanism of catgut embedding therapy for chronic atrophic gastritis.Methods The CAG model of rats was replicated with N-methyl-N’-nitro-N-nitrosoguanidine( MNNG),and the rats were divided into catgut embedding group( 16 rats) and model group( 15 rats),and a blank control group( 15 rats) was established in advance.All three groups were fed with distilled water combined with clean ordinary feed.The catgut embedding group added catgut embedding therapy,blank group and model group cooperated with rats in catgut embedding group to grab and bind at the same time and with the same intensity,without any treatment until the end of the experimental course of treatment.After the course of treatment was completed,the plasma gastrin-17( G-17),VEGF and TNF-α contents were detected by enzyme-linked immunosorbent assay( ELISA).Results The expressions of serum G-17,VEGF and TNF-α in the model group and the embedding group,the model group and the blank group were statistically significant( P > 0.05).There was no significant difference in the expressions of serum G-17,VEGF and TNF-α between the embedding group and the blank group( P > 0.05).The order of serum G-17 expression from weak to strong was model group,embedding group,blank group.The order of expressions of serum VEGF and TNF-α from weak to strong was blank group,embedding group,model group.Conclusion Embedding may play a role in the treatment of CAG by regulating the expressions of G-17,VEGF and TNF-α.