萎缩性胃炎患者外周血TLR4 MyD88 NF-κB及PG水平变化与Hp感染病变进程及炎症反应的关系

doi:10.3969/j.issn.1006-6233.2023.10.008

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Abstract Objective: To investigate the changes in the expression of serum Toll-like receptor 4 (TLR4), myeloid differentiation factor-88 (MyD88), nuclear factor κB (NF-κB), and pepsinogen (PG Ⅰ, PG Ⅱ) in patients with atrophic gastritis, and their clinical significance. Methods: A total of 98 patients with atrophic gastritis confirmed by gastroscopy taking pathological tissue examination during the period from December 2020 to March 2023 in the First Hospital of Yulin City were selected as Group A, 100 patients with non-atrophic gastritis confirmed by examination during the same period were selected as Group B, and 100 volunteers for health physical examination were selected as Group C. The serum of the study subjects of the three groups were examined and compared with those of the three groups in terms of the expression changes of serum TLR4, MyD88, NF- κB, PGⅠ, PGⅡ, interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) levels of the three study groups, and stratified according to whether the patients were co-infected with Hp infection or not, and endoscopic grading criteria of atrophic gastritis for comparing the differences of the above indexes. Results: The TLR4, MyD88, NF-κB, PGII, IL-6, IL-1β, and TNF-α of patients in Group A were significantly higher than those in Groups B and C, and the PGⅠ assay was significantly lower than those in Groups B and C, with a statistically significant difference (P<0.05); the TLR4, MyD88, NF- κB, PGII, IL-6, IL-1β, and TNF-α were significantly higher than those in group B, and the values of PGⅠ assay were significantly lower than those in group C, and the difference was statistically significant (P<0.05); in the Hp-positive group, the values of TLR4, MyD88, PGII, IL-6, IL-1β, and TNF-α were significantly higher than those in the Hp-negative group, and the values of PGⅠ assay were significantly lower than those in the Hp-negative group, and the difference was statistically significant (P<0.05); TLR4, MyD88, NF-κB , PGⅡ, IL-6, IL-1β, and TNF-α of patients with grade III lesions were significantly higher than those of patients with grades II and I, and the values of PGⅠ assay were significantly lower than those of patients with grades II and I, and the difference was statistically significant (P<0.05); TLR4 of patients with grade II TLR4, MyD88, NF-κB , PGII, IL-6, IL-1β, TNF-α were significantly higher in patients with grade II lesions than in patients with grade I. The PGⅠ assay was significantly lower than that in patients with grade I, and the difference was statistically significant (P<0.05); TLR4, MyD88, NF-κB with IL-6, IL-1β, and TNF-α were all significantly positively correlated (P<0.05), and there was no significant correlation between PGII and PGⅠ and IL-6, IL-1β, and TNF-α (P>0.05). Conclusion: The TLR4/MyD88/NF-κB pathway is related to the degree of lesions and the occurrence of Hp infection in patients with atrophic gastritis, and regulates the severity of inflammatory response in patients to a certain extent.

Key words： Atrophic gastritis Toll like receptor 4 Medullary differentiation factor 88 Nuclear factor κB Pepsinogen

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2023.10.008 OR http://www.hbyxzzs.cn/EN/Y2023/V29/I10/1629

[1] 张琳,张云云.血清胃蛋白酶原联合胃泌素-17检测对早期胃癌的诊断价值[J].川北医学院学报,2020,35(6):1055-1058.
[2] Zheng XJ,Chen PP,Liu Y,et al.Effect of modified danggui shaoyao powder on SOCS3/TLR4 signaling pathway in rats with chronic atrophic gastritis[J].Zhongguo Zhong Yao Za Zhi,2022,47(15):4128-4135.
[3] Youcheng HE,Xiaoling Y,Sihan LI,et al.Therapeutic effect of Qinghuayin against chronic atrophic gastritis through the inhibition of toll or interleukin-1 receptor domain-containing adaptor inducing interferon-β signaling pathway[J].Tradit Chin Med,2022,42(2):221-226.
[4] 中华医学会消化病学分会.中国慢性胃炎共识意见[J].胃肠病学,2013,18(1):24-36.
[5] 贺新国,郭保根.幽门螺杆菌相关萎缩性胃炎的区域耐药性分析[J].海南医学,2021,32(5):571-573.
[6] 李兆申.慢性萎缩性胃炎的早筛、早诊、早治与胃癌的预防[J].中华消化杂志,2021,41(Z1):5-8.
[7] 黎慧娟,陈露,唐畅宇.TLR4/NF-κB/COX-2致炎信号通路对幽门螺杆菌相关性慢性萎缩性胃炎发生、发展的影响及机制研究[J].胃肠病学和肝病学杂志,2020,29(7):773-777.
[8] 杨敬端,何明,吴品.炎症因子IL-33通过mTOR/Akt信号通路调节肥大细胞反应抑制萎缩性胃炎[J].免疫学杂志,2022,38(4):324-331.
[9] Mommersteeg MC,Simovic I,Yu B,et al.Autophagy mediates ER stress and inflammation in Helicobacter pylori-related gastric cancer[J].Gut Microbes,2022,14(1):2015238.
[10] Sakaguchi T,Sugihara T,Ohnita K,et al.Pyloric incompetence associated with helicobactor pylori infection and correlated to the severity of atrophic gastritis[J].Diagnostics (Basel),2022,12(3):572.
[11] Osmola M,Hemont C,Chapelle N,et al.Atrophic gastritis and autoimmunity:results from a prospective,multicenter study[J].Diagnostics (Basel),2023,13(9):1599.
[12] Rugge M,Savarino E,Sbaraglia M,et al.Gastritis:the clinico-pathological spectrum[J].Dig Liver Dis.2021,53(10):1237-1246.