Effect of oxycodone preconditioning on mitochondrion-dependent apoptosis in liver cells during intestinal ischemia-reperfusion in rats
10.3760/cma.j.issn.0254-1416.2018.06.009
- VernacularTitle:羟考酮预处理对大鼠肠缺血再灌注时线粒体途径肝细胞凋亡的影响
- Author:
Guoqing JING
1
;
Yun WI
;
Qingtao MENG
;
Zhongyuan XIA
Author Information
1. 430060,武汉大学人民医院麻醉科
- Keywords:
Oxycodone;
Reperfusion injury;
Intestines;
Hepatocytes;
Apoptosis;
Mitochondria
- From:
Chinese Journal of Anesthesiology
2018;38(6):672-675
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of oxycodone preconditioning on mitochondrion-dependent apoptosis in liver ceils during intestinal ischemia-reperfusion (I/R) in rats.Methods Fifty-four healthy male Sprague-Dawley rats,weighing 200-300 g,were divided into 9 groups (n=6 each) using a random number table:sham operation group (group S),I/R group,oxycodone preconditioning group (group OP),μ receptor blocker CTOP group (group CTOP),δ receptor blocker naltrindole (NTD) group (group NTD),κ receptor blocker nor-binaltorphimne (BNI) group (group BNI),CTOP plus oxycodone preconditioning group (group CTOP+OP),NTD plus oxycodone preconditioning group (group NTD+ OP),and BN1 plus oxycodone preconditioning group (group BNI+OP).The model of intestinal I/R was established by occluding the superior mesenteric artery for 45 min followed by 2 h reperfusion.Oxycodone 0.5 mg/kg was injected intravenously at 10 min prior to ischemia in OP,COTP+OP,NTD+OP and BNI+ OP groups.COTP 1 mg/kg and NTD 5 mg/kg were injected intravenously at 20 min prior to ischemia in COTP+OP and NTD+OP groups,respectively.BNI 5 mg/kg was injected intravenously at 25 min prior to ischemia in group BNI+OP.CTOP 1 mg/kg and NTD 5 mg/kg were injected intravenously at 10 min prior to ischemia in CTOP and NTD groups,respectively.BNI 5 mg/kg was injected intravenously at 15 min prior to ischemia in group BNI.The superior mesenteric artery was only exposed but not occluded in group S.The rats were sacrificed at 2 h of reperfusion,and livers were removed for determination of apoptosis in liver cells (using TUNEL) and expression of Bcl-2 and caspase-3 in liver tissues (by immunohistochemistry).The apoptosis index (AI) was calculated.Results Compared with group S,AI was significantly increased,the expression of Bcl-2 was down-regulated and the expression of caspase-3 was up-regulated in the other eight groups (P＜0.05).Compared with group I/R,AI was significantly decreased,the expression of Bcl-2 was up-regulated,and the expression of caspase-3 was down-regulated in group OP (P＜0.05).Compared with group OP,AI was significantly increased,Bcl-2 expression was down-regulated,and caspase-3 expression was up-regulated in COTP+OP,NTD+OP and BNI+OP groups (P＜0.05).Conclusion The mechanism by which oxycodone preconditioning activates μ,δ and κ receptors and reduces intestinal I/R injury may be related to inhibiting mitochondrion-dependent apoptosis in rats.
