传统中药联合标准三联疗法治疗幽门螺杆菌诱发的慢性非萎缩性胃炎及其作用机制

发布时间：2018-11-23 20:42

【摘要】：目的:以传统中药清胃止痛微丸联合标准三联疗法治疗幽门螺杆菌诱发的慢性非萎缩性胃炎,采用高通量PCR芯片技术检测炎症相关基因的差异表达情况,阐明其作用机制。方法:选取10例慢性非萎缩性胃炎并发幽门螺杆菌感染患者为治疗组,以清胃止痛微丸联合三联疗法对患者进行治疗14d;随机选取健康者10人作为健康对照组。分别于治疗前后采集研究对象的外周血,应用QIAGEN人类抗菌应答PCR芯片进行外周血总RNA检测,分析治疗前后84个炎症相关基因的差异表达情况。结果:筛选出20个炎症相关基因差异表达。与健康对照组比较,治疗组患者治疗前差异表达的20个基因表达水平明显上调(Fold-change2);与治疗前比较,治疗后该20个基因表达水平下调,且11个基因接近健康对照组水平(Fold-change2)。差异表达基因中包括NLRP3炎性复合体相关基因,其中治疗组患者治疗前CASP1、IL1B、NLRP3和PYCARD基因表达水平与健康对照组比较明显上调(P0.05),治疗组患者治疗后CASP1、IL1B、NLRP3和PYCARD基因的表达水平与治疗前比较明显下调(P0.05)。结论:清胃止痛微丸联合三联疗法治疗幽门螺旋杆菌诱发的慢性非萎缩性胃炎的机制可能是通过抑制慢性非萎缩性胃炎患者NLRP3炎性复合体相关基因的表达,干扰机体与抗菌应答相关的先天性免疫应答,从而起到治疗作用。
[Abstract]:Aim: to treat chronic non-atrophic gastritis induced by Helicobacter pylori with traditional Chinese medicine Qingwei Zhitong pellet and standard triple therapy. High throughput PCR microarray technique was used to detect the differential expression of inflammatory genes and to elucidate its mechanism. Methods: ten patients with chronic non-atrophic gastritis complicated with Helicobacter pylori infection were selected as treatment group. The peripheral blood samples were collected before and after treatment. The total RNA was detected by QIAGEN human antibacterial response PCR chip. The differential expression of 84 inflammatory genes was analyzed before and after treatment. Results: 20 differentially expressed inflammatory genes were screened. Compared with the healthy control group, 20 differentially expressed genes were significantly up-regulated (Fold-change2) in the treatment group before treatment. After treatment, the 20 genes were down-regulated and 11 genes were close to the healthy control group (Fold-change2). The differentially expressed genes included NLRP3 inflammatory complex related genes. The expression levels of CASP1,IL1B,NLRP3 and PYCARD in the treatment group were significantly higher than those in the healthy control group (P0.05). After treatment, the expression of CASP1,IL1B, in the treatment group was significantly higher than that in the control group (P0.05). The expression levels of NLRP3 and PYCARD genes were significantly down-regulated (P0.05). Conclusion: the mechanism of treating chronic non-atrophic gastritis induced by Helicobacter pylori may be by inhibiting the expression of NLRP3 inflammatory complex gene in patients with chronic non-atrophic gastritis. It interferes with the innate immune response associated with antibacterial response and thus plays a therapeutic role.
【作者单位】： 吉林大学基础医学院病原生物学系;吉林华康药业股份有限公司;
【基金】：吉林省科技厅医药产业发展引导资金资助课题(20150311012YY)
【分类号】：R573.3
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本文编号：2352635