摘要
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 explore the changes of inflammatory cytokines levels,activities of regulators,and insulin resistance index（IRI）of the type 2diabetes patients with Helicobacter pylori infection so as to open up new ideas for further study of pathogenesis of H.pylori infection in the type 2diabetes patients.METHODS From Mar 2010to Jun 2011,totally 260patients who were hospitalized in the department of endocrinology and department of gastroenterology were enrolled in the study and divided into the non-diabetes chronic superficial gastritis H.pylori infection group,the type 2diabetes without H.pylori infection group,and the type 2diabetes complicated with H.pylori infection group according to the status of H.pylori infection,with 65cases in each,meanwhile 65patients without diabetes or stomach illness that matched with the 260cases in age and gender were chosen as the control group,then the serum high sensitive C-reactive protein（hs-CRP）was tested by means of immunofluorescence assay,the levels of serum interleukin-6（IL-6）,interleukin-6（IL-6）,interleukin-1β（IL-1β）,and tumor necrosis factor-α（TNF-α）were determined with the use of ELISA method,the activity of the endogenous nuclear factor-κβ（NF-κβ）in peripheral blood was tested by means of immunohistochemistry method;the fasting plasma glucose level was tested by using the oxidase method;the fasting insulin level was tested with the use of radioimmunoassay,and the H.pylori was detected by means of 13Cbreath test.RESULTS The levels of serum hs-CRP,IL-6,and TNF-αof the type 2diabetes patients complicated with H.pylori infection were respectively（12.25 ±2.37）mg/L,（22.39±3.50）ng/L,and（34.73±5.16）ng/L,significantly higher than those of other three groups,the differences were significant（P＆lt;0.05）.The activity of NF-κβin the peripheral blood of the type 2diabetes patients complicated with H.pylori infection was（129.26±10.83）pg/ml,the IFI 14.75±4.14,significantly higher than those of other three groups（P＆lt;0.05）.The IL-1βlevel was（10.52±2.87）ng/L in the type 2 diabetes complicated with H.pylori infection group,（9.47±1.08）ng/L in the non-diabetes chronic superficial gastritis H.pylori infection group,（9.39±1.14）ng/L in the type 2diabetes without H.pylori infection group, the difference was not significant.CONCLUSION The levels of the inflammatory cytokines are elevated under the joint action of hyperglycemia and H.pylori,which can activate the NF-κβ,induce the insulin resistance,and lead to or accelerate the emergence and development of H.pylori infection,consequently,the NF-κβcan be used as a novel drug target for anti-inflammation therapy for patients with H.pylori infection.
出处
《中华医院感染学杂志》
CAS
CSCD
北大核心
2014年第9期2211-2213,共3页
Chinese Journal of Nosocomiology
基金
湖北省卫生厅科研基金资助项目(JX6B88)
关键词
糖尿病
幽门螺杆菌
炎症因子
调控因子
Diabetes mellitus
Helicobacter pylori
Inflammatory cytokine
Regulator
