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目的探讨2型糖尿病(T2DM)患者幽门螺杆菌(Hp)感染的炎症因子水平、调控因子活性及胰岛素抵抗指数(IRI)的变化,为深入研究T2DM合并Hp感染的发病机制和开发治疗药物提供新思路。方法选择2010年3月-2011年6月医院内分泌科和消化内科住院患者共260例,根据是否感染Hp分为非糖尿病慢性浅表性胃炎Hp感染组、2型糖尿病无Hp感染组、2型糖尿病合并Hp感染组,每组各65例,另选在此期间与之年龄、性别等相匹配的65例非糖尿病、非胃病患者为对照组;血清超敏C-反应蛋白(hs-CRP)采用免疫荧光分析法检测,血清白介素6(IL-6)、白介素1β(IL-1β)、肿瘤坏死因子-α(TNF-α)水平采用ELISA法检测;外周血内源性核因子-κβ(NF-κβ)活性采用免疫组织化学法检测;采用氧化酶法检测空腹血糖(FPG),放射免疫法检测空腹胰岛素(FINS);13 C呼气试验测定检测Hp。结果 2型糖尿病合并Hp感染组血清hs-CRP、IL-6、TNF-α水平分别为(12.25±2.37)mg/L、(22.39±3.50)ng/L、(34.73±5.16)ng/L,均显著高于其他3组,差异有统计学意义(P<0.05);2型糖尿病合并Hp感染组外周血NF-κβ活性为(129.26±10.83)pg/ml,IRI为14.75±4.14,也显著高于其他3组,差异有统计学意义(P<0.05);但其IL-1β水平为(10.52±2.87)ng/L,与非糖尿病慢性浅表性胃炎Hp感染组的(9.47±1.08)ng/L和2型糖尿病无Hp感染组的(9.39±1.14)ng/L比较,差异无统计学意义。结论在高血糖和Hp共同作用下,炎症因子水平升高,可以激活NF-κβ,诱导产生胰岛素抵抗,引起和加速2型糖尿病患者幽门螺杆菌感染的发生和发展;因此,NF-κβ可作为2型糖尿病合并幽门螺杆菌感染患者抗炎治疗中新型的抗炎靶点。
Objective To investigate the changes of inflammatory cytokines, regulatory factor activities and insulin resistance index (IRI) in Helicobacter pylori (Hp) infection in type 2 diabetes mellitus (T2DM) patients. To explore the pathogenesis of T2DM complicated with Hp infection and to provide new therapeutic drugs Ideas. Methods From March 2010 to June 2011, a total of 260 hospitalized patients with endocrinology and gastroenterology in our hospital were divided into non-diabetic chronic superficial gastritis Hp infection group, type 2 diabetes without Hp infection group, type 2 diabetes mellitus group Sixty-five patients with diabetes mellitus and Hp infection were enrolled in this study. Sixty-five nondiabetic and non-gastric patients, matched with their age and gender, were selected as the control group. Serum high-sensitivity C-reactive protein (hs-CRP) The levels of serum IL-6, IL-1β and TNF-α were detected by immunofluorescence assay. The levels of endogenous nuclear factor-κβ The activity of NF-κβ was detected by immunohistochemical method. Fasting plasma glucose (FPG) was measured by oxidase method and fasting insulin (FINS) by radioimmunoassay. The 13 C breath test was used to detect Hp. Results The serum levels of hs-CRP, IL-6 and TNF-α in type 2 diabetic patients with Hp infection were (12.25 ± 2.37) mg / L and (22.39 ± 3.50) ng / L and (34.73 ± 5.16) (P <0.05). The activity of NF-κB in peripheral blood of type 2 diabetic patients with Hp infection was (129.26 ± 10.83) pg / ml and IRI was 14.75 ± 4.14, which was also significantly higher than those in other 3 groups (P <0.05), but the level of IL-1β was (10.52 ± 2.87) ng / L, which was significantly higher than that of non-diabetic chronic superficial gastritis (9.47 ± 1.08) There was no significant difference between the two groups (9.39 ± 1.14) ng / L for type 2 diabetes without Hp infection. Conclusion The combination of hyperglycemia and Hp may increase the level of inflammatory cytokines and activate NF-κβ to induce insulin resistance and cause and accelerate the occurrence and development of Helicobacter pylori infection in type 2 diabetic patients. Therefore, NF-κβ may act as New Anti-inflammatory Targets for Anti-inflammatory Therapy in Type 2 Diabetes with Helicobacter Pylori Infection.