發(fā)布時(shí)間：2018-11-23 20:42

【摘要】：目的:以傳統(tǒng)中藥清胃止痛微丸聯(lián)合標(biāo)準(zhǔn)三聯(lián)療法治療幽門螺桿菌誘發(fā)的慢性非萎縮性胃炎,采用高通量PCR芯片技術(shù)檢測炎癥相關(guān)基因的差異表達(dá)情況,闡明其作用機(jī)制。方法:選取10例慢性非萎縮性胃炎并發(fā)幽門螺桿菌感染患者為治療組,以清胃止痛微丸聯(lián)合三聯(lián)療法對患者進(jìn)行治療14d;隨機(jī)選取健康者10人作為健康對照組。分別于治療前后采集研究對象的外周血,應(yīng)用QIAGEN人類抗菌應(yīng)答PCR芯片進(jìn)行外周血總RNA檢測,分析治療前后84個(gè)炎癥相關(guān)基因的差異表達(dá)情況。結(jié)果:篩選出20個(gè)炎癥相關(guān)基因差異表達(dá)。與健康對照組比較,治療組患者治療前差異表達(dá)的20個(gè)基因表達(dá)水平明顯上調(diào)(Fold-change2);與治療前比較,治療后該20個(gè)基因表達(dá)水平下調(diào),且11個(gè)基因接近健康對照組水平(Fold-change2)。差異表達(dá)基因中包括NLRP3炎性復(fù)合體相關(guān)基因,其中治療組患者治療前CASP1、IL1B、NLRP3和PYCARD基因表達(dá)水平與健康對照組比較明顯上調(diào)(P0.05),治療組患者治療后CASP1、IL1B、NLRP3和PYCARD基因的表達(dá)水平與治療前比較明顯下調(diào)(P0.05)。結(jié)論:清胃止痛微丸聯(lián)合三聯(lián)療法治療幽門螺旋桿菌誘發(fā)的慢性非萎縮性胃炎的機(jī)制可能是通過抑制慢性非萎縮性胃炎患者NLRP3炎性復(fù)合體相關(guān)基因的表達(dá),干擾機(jī)體與抗菌應(yīng)答相關(guān)的先天性免疫應(yīng)答,從而起到治療作用。
[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.
【作者單位】： 吉林大學(xué)基礎(chǔ)醫(yī)學(xué)院病原生物學(xué)系;吉林華康藥業(yè)股份有限公司;
【基金】：吉林省科技廳醫(yī)藥產(chǎn)業(yè)發(fā)展引導(dǎo)資金資助課題(20150311012YY)
【分類號】：R573.3
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本文編號：2352635