中国病理生理杂志2016，Vol.32Issue(11)：2026-2030,5.DOI:10.3969/j.issn.1000-4718.2016.11.018
异丙酚通过抑制JAK/STAT通路减轻肝冷缺血再灌注大鼠肾损伤∗
Propofol attenuates kidney injury after liver cold ischemia/reperfusion in rats via inhibiting JAK/STAT signaling activation
摘要
Abstract
[ ABSTRACT] AIM:To investigate the role of Janus kinase/signal transducer and STAT) signaling pathway in propofol ( Pro)-induced reduction of kidney injury after liver c METHODS:Sprague-Dawley rats were assigned randomly to 4 groups ( n=8 each group group);liver cold ischemia/reperfusion model group ( I/R group);propofol group ( Pro gr ·kg-1 ·h-1 was infused continuously for 30 min via right femoral vein 5 min before rep group ( AG490 group):AG490 at dose of 10 mg/kg was applied by intraperitoneal injectio model. The rats were sacrificed at 6 h after reperfusion. Blood samples and kidney tissues concentrations of creatinine ( Cr ) , blood urea nitrogen ( BUN ) , interleukin-6 ( IL-6 ) ( TNF-α) , and the tissue levels of malondialdehyde ( MDA) and superoxide dismutase ( S the renal tissues and nephritic cell apoptosis were analyzed, the damage of the renal tubule (AI) was calculated. The protein levels of p-JAK2, p-STAT1 and p-STAT3 were det SULTS:Compared with sham group, the levels of Cr, BUN, IL-6, TNF-αand MDA, AI were significantly increased, the SOD activity was decreased, and the protein levels of p were up-regulated in I/R group (P<0. 05). Compared with I/R group, the levels of Cr, AI, and renal tubular damage score were significantly decreased, the SOD activity was inc activator of transcription ( JAK/old ischemia/reperfusion in rats. ): sham operation group ( sham oup):propofol at dose of 20 mg erfusion; JAK2 inhibitor AG490 n 30 min before establishing the were obtained to detect the serum and tumor necrosis factor-alpha OD) . The pathologic changes of s was scored and apoptotic index ermined by Western blot. RE-, and renal tubular damage score-JAK2, p-STAT1 and p-STAT3 BUN, IL-6, TNF-α and MDA, reased, and the protein levels of p-JAK2, p-STAT1 and p-STAT3 was down-regulated in Pro group and AG490 group (P<0. 05). CONCLUSION:Propo-fol reduces kidney injury induced by liver cold ischemia/reperfusion, and the mechanism is possibly associated with inhibi-ting the JAK/STAT pathway activation.关键词
异丙酚/缺血再灌注损伤/JAK/STAT信号通路/肝/肾Key words
Propofol/Ischemia/reperfusion injury/JAK/STAT signaling pathway/Liver/Kidney分类
医药卫生引用本文复制引用
王菲,喻文立,贾莉莉,顾向前,翁亦齐,杜洪印..异丙酚通过抑制JAK/STAT通路减轻肝冷缺血再灌注大鼠肾损伤∗[J].中国病理生理杂志,2016,32(11):2026-2030,5.基金项目
天津市卫生行业重点攻关项目(No.13KG105) （No.13KG105）
天津市卫生局科技基金(No.2011KY12) （No.2011KY12）
天津市应用基础研究计划面上项目(No.05YFJMJC14800) （No.05YFJMJC14800）
