Abstract：【Objective】To evaluate the effect of remifentanil preconditioning on the apoptosis of renal cells and expressions of Bcl-2 and Caspase3 after hepatic ischemia reperfusion in rats. 【Methods】Seventy-two adult male SD rats were randomly divided into three equal groups (n=24): the sham operation group (group S), ischemia reperfusion group (group I/R), and remifentanil group (group RPC). According to 4 different time points of ischemia and reperfusion [ischemia for 30 min (T1), reperfusion for 1h (T2), 3h (T3) and 6h (T4)], the rats were further subdivided into 4 subgroups within each group: S1, S2, S3, S4; IR1, IR2, IR3, IR4,; and RPC1, RPC2, RPC3, RPC4. The Hepatic ischemia reperfusion model in rats was established using Pringle's maneuver method. The serum levels of alanine aminotransferase (ALT) and creatinine (Cr) were examined at each time point mentioned above. After 6 hours of reperfusion, the pathological changes in the kidneys were observed. TUNEL staining was used to examine cell apoptosis, and Western blot was employed to examine protein expressions of Bcl-2 and Caspase3 in renal tissues of each group. 【Results】 Serum ALT and creatinine levels in the I/R group and RPC group increased after 30 min of ischemia-these changes were significantly higher than that in the S group (P<0.05). However, levels in RPC group were lower than those in the I/R group (P<0.05). The renal tissue structure of the rats in group S was normal. In the IR group, there were different degrees of pathological damage of renal tissue: renal tubular epithelial cell swelling, lack of structure, nucleus condensation, necrotic exfoliated epithelial cells, and inflammatory cell infiltration. The pathological damage was obviously improved following remifentanil preconditioning in RPC group. TUNEL staining revealed that there were significantly lower apoptotic cells in the S group than those in the I/R group and the RPC group (P<0.05), and that the degree in the I/R group was much higher than that in the RPC group (P<0.05). Western blot detection of apoptotic protein showed that the expression of Bcl-2 and Caspase3 in the I/R group were higher than those in the S group (P<0.05). After Remifentanil preconditioning in RPC group, the expression of Bcl-2 increased but Caspase-3 expression decreased (P<0.05).【Conclusion】 Remifentanil preconditioning has a protective effect on renal injury after hepatic ischemia reperfusion, and the protective mechanism may be involved in the regulation of renal cell apoptosis and the expression of Bcl-2 and Caspase-3.
孙辉平,杨金凤,邹双发,张秦雅,彭艳华,肖卫强. 瑞芬太尼预处理对鼠肝缺血再灌注损伤时肾细胞凋亡及Bcl-2、caspase-3的影响[J]. 医学临床研究, 2017, 34(6): 1115-1118.
SUN Hui-ping, YANG Jin-feng, ZOU Shuang-fa,et al. Effect of Remifentanil Preconditioning on the Apoptosis of Renal Cells and Expression of Bcl-2 and Caspase3 after Hepatic Ischemia Reperfusion in Rats. JOURNAL OF CLINICAL RESEARCH, 2017, 34(6): 1115-1118.
[1] Park SW, Kim M, Brown KM,et al. Paneth cell-derived interleukin-17A causes multiorgan dysfunction after hepatic ischemia and reperfusion injury[J].Hepatology,2011,53(5): 1662-1675. [2] Park SW, Chen SW, Kim M, et al. Protection against acute kidney injury via a1 adenosine receptor-mediated akt activation reduces liver injury after liver ischemia and reperfusion in mice[J].J Pharmacol Exp Ther,2010, 333(3): 736-747. [3] Zhou L, Yao X, Chen Y. Dexamethasone pretreatment attenuates lung and kidney injury in cholestatic rats induced by hepatic ischemia/ reperfusion[J].Inflammation,2012, 35 (1): 289-296. [4] Gujral JS,Bucci TJ,Farhood A,et al. Mechanism of cell death during warm hepatic ischemia reperfusion in rats apoptosis or necrosis[J].Hepatology,2001,33(2):397-405. [5] Yang LQ1, Tao KM, Liu YT, et al. Remifentanil preconditioning reduces hepatic ischemia reperfusion injury in rats via inducible nitric oxide synthase expression[J].Anesthesiology,2011, 114 (5): 1036-1047. [6] Vianna PT, Castiglia YM, Braz JR, et al. Remifentanil, isoflurane, and preconditioning attenuate renal ischemia/reperfusion injury in rats[J].Transplant Proc,2009, 41(10):4080-4082. [7] Dou MY,Wu H,Zhu HJ,et al. Remifentanil preconditioning protects rat cardiomyocytes against hypoxia-reoxygenation injury via δ-opioid receptor mediated activation of PI3K/Akt and ERK pathways[J].Eur J Pharmacol,2016 , 789(15):395-401. [8] Davis CL, Gonwa TA, Wilkinson AH. Pathophysiology of renal disease associated with liver disorders: implications for liver transplantation[J].Liver Transpl,2002 , 8(2):91-109. [9] Kwon JY, Park BS, Kim YH, et al. Remifentanil protects human keratinocytes against hypoxia-reoxygenation injury through activation of autophagy[J].PLoS One,2015,10(1): e0116982. [10] Che X, Wang X, Zhang J, et al. Vitexin exerts cardioprotective effect on chronic myocardial ischemia/reperfusion injury in rats via inhibiting myocardial apoptosis and lipid peroxidation[J].Am J Transl Res,2016,8(8): 3319-3328. [11] Jiang CJ, Wang ZJ, Zhao YJ, et al. Erythropoietin reduces apoptosis of brain tissue cells in rats after cerebral is chemia/reperfusion injury: a characteristic analysis using magnetic resonance imaging [J].Neural Regen Res,2016 ,11(9): 1450-1455. [12] Havasi A, Borkan SC. Apoptosis and acute kidney injury [J].Kidney int,2011, 80(1): 29-40. [13] Zhang L, Gan W, An G. Influence of Tanshinone IIa on heat shock protein70, Bcl-2 and Bax expression in rats with spinal ischemia/reperfusion injury [J].Neural Regen Res,2012 , 7(36): 2882-2888. [14] Pradelli LA, Beneteau M, Ricci J. Mitochondrial control of caspase-dependent and -independent cell death[J].Cellul Molecul Life Sci,2010, 67(10):1589-1597. [15] Voutsadakis IA.Apoptosis and the pathogenesis of lymphoma[J].Acta Oncol,2000,39(2): 151-156. (本文编辑:邓丽萍) [收稿日期] 2016-12-19
2017, Vol. 34 
