TLR4介导大鼠肾脏缺氧复氧炎症反应依赖于MyD88

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 factor α,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.

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

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.