双歧杆菌缓解DSS诱导的溃疡性结肠炎作用机制的研究

Study on the mechanism of action of Bifidobacteria in DSS induced UC

目的通过RT-PCR检测IECs中TLR2与TLR4的表达,通过荧光定量PCR检测IECs中IL-1和TNF-α的表达,以对双歧杆菌预防与辅助治疗UC作用机制加以探讨。方法将36只Babl/c小鼠随即分为3组,即正常对照组(N)、DSS诱导组(D)、双歧杆菌喂养组(B)。N组不施加作用,D组生理盐水灌肠2周,并在第2周给以2%的DSS自由饮用;双歧杆菌组双歧杆菌灌肠2周,并在第2周再给以2%的DSS自由饮用。2周后处死小鼠做组织切片和分离IECs并提取IECs中的总RNA,用RT-PCR检测TLR2、TLR4的表达,用Real time RT-PCR检测IL-1和TNF-α表达。结果双歧杆菌组IECs表达TLR2远远高于单纯的DSS诱导组,结果具有统计学意义,而双歧杆菌组IECs表达TLR4、IL-1和TNF-α则远远低于单纯的DSS诱导组,结果具有统计学意义。结论双歧杆菌通过与诱导IECs中TLR2的表达而抑制其TLR4、IL-1和TNF-α的表达,从而达到预防与辅助性治疗DSS诱导的UC作用。

Objectives To detect the expression of TLR2 and TLR4 in IECs with the RT-PCR in UC with or without bifidobacteria administration; and the expression of IL-1 and TNF-α in IECs with the Real time RT-PCR,to determine potential the effect of TLR2 ,TLR4 ,IL-1 and TNF-α in the immunopathogenesis of UC and the Bifidobacteria＇s effects in the UC. Methods Thrity-six Babl/c mice were divided randomly into three groups,namely the normal group（N） ,the DSS induced group（D） and the bifidobacteria given group（B）. There were no treatmen with the N group;The group D were given normal sodium for coloclysis 2 weeks,and from the second week 2% DSS were given for free drink;and the group B were given coloclysis for bifidobacteria 2 weeks, and from the second week 2% DSS were given for free drink. Then the Babl/c mice were put to death and the colonic tissue slice were made for histological changes observation;The IECs＇ total RNA were extracted for the detection of TLR2,TLR4,IL-1 and TNF-α. Results The expression of TLR2 in IECs of the group B were incressed compare with the group N and D（ P 〈0.05） ,but in the group B there were no increased TLR4;In group D there were increased TLR4 compare with the group N and B（P〈0.05） ;The expression of IL-1 and TNF-α in IECs in the group D were incressed compare with the group N and B（P 〈0.05） ,but in the group B there were no increased IL-1 and TNF-α. Conclusion The Bifidobacteria may exert its effect in DSS induced UC by the expression of TLR2,then inhibit the expression of TLR4, IL-1 and TNF-α.