慢性萎缩性胃炎诊疗思想认识及基础研究

目的 通过检测慢性萎缩性胃炎(chronical atrophic gastritis，CAG)患者血、尿小分子蛋白组的变化，探讨CAG脾胃气虚诱导胃腺体细胞凋亡启动、黏膜萎缩的免疫学基础。 方法 选取2010年10月—2011年8月浙江中医药大学附属第一、三医院门诊患者筛选CAG相关蛋白，IL-2、IL-4、IL-6、IL-7、IL-8、IL-10、IL-12、IL-15、IL-17、IL-1β、IL-1Ra、MIF、IFN-γ、SCF。141例研究对象分为正常组30例，CAG组111例(脾胃气虚证32例，脾胃湿热证33例，肝胃不和证46例)。干预3个月，收集血、尿上清，液相蛋白芯片检测。 结果 干预前血液中IL-2、IL-12、IL-17在三个证型中表达降低；IL-4、IL-7、IL-8、IL-1β、IL-1Ra、MIF、IFN-γ，在各证型中升高，尿液中IL-2、IL-4表达升高，IL-6、IL-12、IL-15、IL-17表达降低。由于时间限制，干预后样本量较少，后续扩大干预后样本量收集，试验结果待发表。 结论 脾胃气虚时，免疫小分子蛋白已处于紊乱，致炎与抗炎因子失去平衡。细胞免疫功能下降，Th1/Th2平衡发生向Th2型细胞因子漂移现象。干预后，细胞免疫及分泌功能呈恢复状态、部分萎缩及未发生瘤变的黏膜发生逆转。脾胃气虚是诱导胃腺体细胞凋亡启动、黏膜萎缩的主要病理因素，具有免疫学基础。 

The theories and fundamental research on chronic atrophic gastritis

Objective Via discussion of the immunological basis of apoptosis and atrophy to gastric gland cell and gastric mucosal induced by deficiency of spleen and stomach qi, to detect the changes of small molecular protein in blood and urine of patients with chronical atrophic gastritis. Methods The proteins, including IL-2, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12,IL-15, IL-17, IL-1β, IL-1Ra, MIF, IFN-γ, SCF, were chosen. A total of 111 patients with CAG were selected as study objects and were classified by TCM syndrome type. The distribution of syndromes were 32 cases of deficiency syndrome of spleen and stomach qi, 33 cases of damp-heat syndrome of spleen and stomach, 46 cases of disharmony syndrome of liver and stomach. The 33 cases were included in the control group. The supernatant of blood and urine were collected before and after treatment for three months. Syndrome-related proteome of CAG possessing good specificity and susceptibility will be determined by liquid suspended bio-chip fluorescence detection technique. Results First before treatment, protein change of CAG TCM Syndrome compared with control group were as follows: in blood of CAG patients, the expression of IL-2, IL-12, IL-17 were decreased, and increased with IL-4, IL-7, IL-8, IL-1β, IL-1Ra, MIF, IFN-γ. The expression were decreased with IL-6, IL-12, IL-15, IL-17 in urine, and increased with IL-2, IL-4. Due to few patient case data with drug intervention, large sample test results will be published after the test completion. Conclusions Cytokine network is unbalanced between proinflammatory and anti-inflammatory based on deficiency of spleen and stomach qi. That state of human body makes the immune cell immunocompromised or immune incompetence. The expression of cytokine network tends to shift to type Th2 between Th1 and Th2 balance. After the intervention of Chinese medicine, the immune function of cell will be enhanced. The stomach mucosa of some patients with mild atrophy returns to normal. Spleen and stomach qi deficiency is the main pathological factor of inducing apoptosis and atrophy to gastric gland cell and gastric mucosa on an immunological basis.