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目的 :探讨幽门螺杆菌 (Hp)感染特别是其细胞毒素相关基因 (cagA因子 )与胃粘膜中bcl 2、Bax、p2 1 WAF1、p16 MTS1蛋白表达异常的关系 ,从而从分子水平初步探讨cagA是否为一致癌因子及其可能的致癌的机理。方法 :1、利用血抗Hp IgG、RUT、PCR Hp DNA 3种方法检测 2 70例病人的Hp感染情况及cagA+ Hp感染情况 ;2、利用免疫组化S P法检测胃癌演化系列胃粘膜中bcl 2、Bax、p2 1 WAF1、p16 MTS1蛋白的表达 ;3、利用SPSS统计软件包作统计学分析处理。结果 :1、在CSG、CAG、IM阶段 ,Hp感染促进胃粘膜中bcl 2、Bax的表达 ,cagA因子促进bcl 2、Bax、p2 1 WAF1、p16 MTS1的表达 ,(P <0 0 5 ) ;在胃癌阶段 ,Hp感染与胃腺癌粘膜中bcl 2、p2 1 WAF1、p16 MTS1的低表达相关 (P <0 0 5 ) ,但与cagA因子无关 (P >0 0 5 ) ;2、在男性CSG、CAG、IM系列胃粘膜中bcl 2、Bax表达先高后低 ,与cagA+ Hp感染率呈正相关 ,而 p16 MTS1、p2 1 WAF1表达先低后高 ,与cagA+ Hp感染率呈负相关 (P <0 0 5 )。结论 :Hp的cagA因子可能通过影响癌前病变患者胃粘膜中bcl 2、Bax、p2 1 WAF1、p16 MTS1的表达 ,成为胃腺癌发生的“启动子”之一 ;Hp可能通过非cagA因子途径影响bcl 2、p2 1 WAF1、p16 MTS1的表达 ,进一步影响胃腺癌的
Objective: To investigate the relationship between Helicobacter pylori (Hp) infection, especially its cytotoxin-related gene (cagA factor), and the abnormal expression of bcl-2, Bax, p21WF1, and p16 MTS1 in the gastric mucosa, so as to investigate whether cagA is preliminary from the molecular level. For consistent cancer factors and their possible carcinogenic mechanisms. Methods:1. Hp infection and cagA+ Hp infection in 270 patients were detected by blood anti-Hp IgG, RUT, and PCR Hp DNA; 2. bcl 2 was detected in gastric mucosa by SP immunohistochemistry. , Bax, p21, WAF1, p16 MTS1 protein expression; 3, using SPSS statistical software package for statistical analysis. Results:1. In the stages of CSG, CAG and IM, Hp infection promoted the expression of bcl 2 and Bax in gastric mucosa, and cagA factor promoted the expression of bcl 2, Bax, p 2 1 WAF1 and p16 MTS1, (P <0 05). In the gastric cancer stage, Hp infection was associated with low expression of bcl 2, p2 1 WAF1, and p16 MTS1 in mucosa of gastric adenocarcinoma (P <0 05), but not cagA factor (P> 0 05); 2. In male CSG The expression of bcl 2 and Bax in the gastric mucosa of CAG and IM groups was firstly high and then low, which was positively correlated with the rate of cagA + Hp infection, while the expression of p16 MTS1, p21 WAF1 was low and high first, and negatively correlated with the cagA + Hp infection rate (P < 0 0 5 ). CONCLUSION: Hg cagA may play a role in the development of gastric adenocarcinoma by affecting the expression of bcl-2, Bax, p2 1 WAF1 and p16 MTS1 in the gastric mucosa of precancerous lesions. Hp may be affected by non-cagA pathways. Expression of bcl 2, p2 1 WAF1, and p16 MTS1 further influences gastric adenocarcinoma