TLR4介导大鼠肾脏缺氧复氧炎症反应依赖于MyD88  

TLR4 Mediates Renal Hypoxia /reoxygenation Inflammatory Response via MyD88-dependent Pathway

作　　者：尹金凤[1] 刘秀娟[2] 沈江山[1] 周阳[1] 尹秀英[2] 

机构地区：[1]南昌大学第四附属医院肾内科,南昌330002 [2]解放军第九四医院肾内科,南昌330002

出　　处：《中国中西医结合肾病杂志》2014年第1期16-19,共4页Chinese Journal of Integrated Traditional and Western Nephrology

基　　金：国家自然科学基金资助项目(No.81260114);南京军区医药卫生科研基金资助项目(No.2007151193)

摘　　要：目的:探讨MyD88是否参与了TLR介导大鼠肾脏缺氧复氧(hypoxia/reoxygenation,H/R)引起的炎症反应。方法:体外分离获得Wistar大鼠原代肾小管上皮细胞(proximal tubule epithelial cells,PTECs),建立H/R模型。采用TLR4siRNA干扰PTECs,检测白细胞介素8(interleukin-8,IL-8)和肿瘤坏死因子α(tumor necrosis factorα,TNF-α)的表达。之后,加入髓样分化因子88(myeloid differentiation factor 88,MyD88)的抑制剂ST2825后,检测IL-8和TNF-α的表达。结果:TLR4表达沉默后,IL-8、TNF-α和MyD88的表达均显著下降(P<0.05);加入ST2825后,IL-8、TNF-α和MyD88的表达均显著下降(P<0.05),且抑制MyD88活性后显著降低细胞的凋亡水平(P<0.05)。结论:MyD88参与了TLR4介导的大鼠肾脏缺氧复氧引起的炎症反应。ABSTRACT Objective： To investigate whether myeloid differentiation factor 88 （ MyD88 ） was involved in Toll like receptor 4 （TLR 4） induced hypoxia/reoxygenation （H/R） inflammatory response. Methods： Primary renal tubular epithehal cells （PTECs） in Wistar rat was isolated. The model of hypoxia/reoxygenation was established. The TLR4 siRNA was transfected into PTECs, then interleukin 8 （interleukin 8, IL- 8） and tumor necrosis factor ct （tumor necrosis factor ct, TNF ct） expression were analyzed. The myeloid differentiation factor 88 （ myeloid differentiation factor 88, MyD88） inhibitor ST2825 was added to PTECs cells, the expres sion of IL 8 and TNF was detected. Results ： The expression of IL 8, TNFc and MyD88 were significantly decreased （ P 〈 0.05） by TLR4 knockdown. Likewise, the expression of IL 8, TNFc and MyD88 were significantly inhibited （ P 〈 0.05 ） by ST2825. The inhibition of MyD88 significantly suppressed the apoptosis of PTECs following IL/R injury. Conclusion： MyD88 was in volved in TLR4 mediated renal hypoxia/reoxygenation induced inflammatory response.

关 键 词：肾小管上皮细胞 缺氧复氧 TLR4 MYD88 炎症反应 

分 类 号：R699.2[医药卫生—泌尿科学]