摘要
目的:探讨缺血性急性肾功能衰竭(IARF)大鼠血清TNF-α水平、肾小管上皮细胞中Fas和Bcl-2的表达及细胞凋亡情况,分析它们在IARF发病机制中的作用。方法:用无损伤动脉夹夹闭大鼠双侧肾蒂40min制作IARF模型,观察缺血再灌注(IR)后2、6、12、24和48h时血清TNF-α及肌酐(SCr)水平,观察各时间点肾脏组织的病理学变化,观察IR12h时肾小管上皮细胞Fas、Bcl-2表达及细胞凋亡。结果:IR12h时肾小管上皮细胞凋亡明显,以皮髓交界处为著,阳性细胞率增加,P<0.01;IR12h时,血清TNF-α和SCr明显增多,P<0.01;IR12h时肾小管上皮细胞Fas表达增加(P<0.01),Bcl-2表达减少(P<0.01);IR各各时间点肾组织均有不同程度的细胞破坏,以IR6h和12h最严重。结论:IR所致的IARF动物模型中存在细胞凋亡的病理改变,严重影响肾功能;血清TNF-α可能通过上凋Fas和下调Bcl-2影响肾小管上皮细胞的凋亡过程。
Objective： To investigate serum TNF-α content, apoptosis, and expression of Fas and Bcl-2 in renal tubular epithelia cells （RTEC）of ischemic acute renal failure （IARF） rat, and to analyze their effects in IARF pathogenesy. Methods： SD rat model of IARF was set up by occluding of bilateral renal pedicle for 40 min and following reperfusion. Serum creatine （SCr） and TNF-α, and kidney tissue pathological changes were observed at time points of 2h, 6h, 12h, 24h, and 48h after ischemia-reperfusion （IR）. At 12h after IR, the expression of Fas, and Bcl-2 in renal tubular epithelia cells and cell apoptosis were investigated. Result： In 12h after IR, cell apoptosis was obvious, specially at the juncture of cortex and medulla showing increased positive rate （P 〈 0. 01 ）. Serum SCr and TNF-α significantly raised （ P 〈 0.01 ）, and in RTEC, Fas expression increased （ P 〈 0.01 ） while that of Bcl-2 deceased （ P 〈 0.01 ） ; Different degrees of cell destroy were found at different time points, and it＇s most serious at 6 h and 12 h. Conclusion： The pathological changes of cell apoptosis
occur in IR caused IARF animal model and influence renal function severely; Serum TNF-α might affect apoptosis process in RTEC by up-regulate Fas and down-regulate Bcl-2.
出处
《贵阳医学院学报》
CAS
2009年第5期508-511,共4页
Journal of Guiyang Medical College
