Futrakul Narisa, Siriviriyakul Prasong, Panichakul Tasanee, Butthep Punnee, Patumraj Suthiluk, Futrakul Prasit
Department of Physiology, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
Clin Hemorheol Microcirc. 2003;29(3-4):469-73.
Glomerular endothelial cell dysfunction (GED) with defective release of vasodilator has been delineated in nephrosis (NS) in vivo and in vitro studies. In NS with focal segmental glomerulosclerosis (FSGS), an immunocirculatory balance may be impaired due to defective anti-inflammatory cytokine. This study aimed at simultaneous determination of both proinflammatory cytokine (tumor necrosis factor alpha) and an anti-inflammatory cytokine (interleukin-10) in NS with FSGS. An endothelial cell cytotoxicity (ECC) was also examined using nephrotic serum. It was shown that (1) the initial endothelial cell cytotoxicity was significantly different from the control, (2) ratio between tumor necrosis alpha and interleukin-10 was significantly elevated, and (3) intrarenal hemodynamics was changed significantly.
在体内和体外研究中，已明确肾病（NS）存在肾小球内皮细胞功能障碍（GED），其血管舒张因子释放存在缺陷。在伴有局灶节段性肾小球硬化（FSGS）的NS中，由于抗炎细胞因子缺陷，免疫循环平衡可能受到损害。本研究旨在同时测定伴有FSGS的NS中促炎细胞因子（肿瘤坏死因子α）和抗炎细胞因子（白细胞介素-10）。还使用肾病血清检测了内皮细胞细胞毒性（ECC）。结果显示：（1）初始内皮细胞细胞毒性与对照组有显著差异；（2）肿瘤坏死因子α与白细胞介素-10的比值显著升高；（3）肾内血流动力学发生显著变化。
