摘要
AIM: To evaluate preventative effects of ischemic preconditioning(IP) in a rat model of intestinal injury induced by ischemia-reperfusion(IR).METHODS: Male Sprague-Dawley rats(250-300 g) were fasted for 24 h with free access to water prior to the operation.Eighteen rats were randomly divided into three experimental groups: S group(n = 6),rats were subjected to isolation of the superior mesenteric artery(SMA) for 40 min,then the abdomen was closed; IRgroup(n = 6),rats were subjected to clamping the SMA 40 min,and the abdomen was closed followed by a 4-h reperfusion; IP group(n = 6) rats underwent three cycles of 5 min ischemia and 5 min reperfusion,then clamping of the SMA for 40 min,then the abdomen was closed and a 4-h reperfusion followed.All animals were euthanized by barbiturate overdose(150 mg/kg pentobarbital sodium,i.v.) for tissue collection,and the SMA was isolated via median abdominal incision.Intestinal histologic injury was observed.Malondialdehyde(MDA),myeloperoxidase(MPO) and tumor necrosis factor(TNF)-a concentrations in intestinal tissue were measured.Intercellular adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 expression,as well as nuclear factor(NF)-κB activity and expression in intestinal tissue were also determined.RESULTS: Compared with the IR group,IP reduced IR-induced histologic injury of the intestine in rats(2.00 ± 0.71 vs 3.60 ± 0.84,P < 0.05).IP significantly inhibited the increase in MDA content(5.6 ± 0.15 μmol/L vs 6.84 ± 0.18 μmol/L,P < 0.01),MPO activity(0.13 ± 0.01 U/L vs 0.24 ± 0.01 U/L,P < 0.01),and TNF-a levels(7.79 ± 2.35 pg/m L vs 10.87 ± 2.48 pg/m L,P < 0.05) in the intestinal tissue of rats.IP also markedly ameliorated the increase in ICAM-1(204.67 ± 53.27 vs 353.33 ± 45.19,P < 0.05) and VCAM-1(256.67 ± 58.59 vs 377.33 ± 41.42,P < 0.05) protein expression in the intestinal tissues.Additionally,IP remarkably decreased NF-κB activity(0.48 ± 0.16 vs 0.76 ± 0.22,P < 0.05) and protein expression(320.23 ± 38.16 vs 520.76 ± 40.53,P < 0.01) in rat intestinal tissue.CONCLUSION: IP may protect against IR-induced intestinal injury by attenuation of the neutrophilendothelial adhesion cascade via reducing ICAM-1 and VCAM-1 expression and TNF-a-induced NF-κB signaling pathway activity.
AIM: To evaluate preventative effects of ischemic preconditioning(IP) in a rat model of intestinal injury induced by ischemia-reperfusion(IR).METHODS: Male Sprague-Dawley rats(250-300 g) were fasted for 24 h with free access to water prior to the operation.Eighteen rats were randomly divided into three experimental groups: S group(n = 6),rats were subjected to isolation of the superior mesenteric artery(SMA) for 40 min,then the abdomen was closed; IRgroup(n = 6),rats were subjected to clamping the SMA 40 min,and the abdomen was closed followed by a 4-h reperfusion; IP group(n = 6) rats underwent three cycles of 5 min ischemia and 5 min reperfusion,then clamping of the SMA for 40 min,then the abdomen was closed and a 4-h reperfusion followed.All animals were euthanized by barbiturate overdose(150 mg/kg pentobarbital sodium,i.v.) for tissue collection,and the SMA was isolated via median abdominal incision.Intestinal histologic injury was observed.Malondialdehyde(MDA),myeloperoxidase(MPO) and tumor necrosis factor(TNF)-a concentrations in intestinal tissue were measured.Intercellular adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 expression,as well as nuclear factor(NF)-κB activity and expression in intestinal tissue were also determined.RESULTS: Compared with the IR group,IP reduced IR-induced histologic injury of the intestine in rats(2.00 ± 0.71 vs 3.60 ± 0.84,P < 0.05).IP significantly inhibited the increase in MDA content(5.6 ± 0.15 μmol/L vs 6.84 ± 0.18 μmol/L,P < 0.01),MPO activity(0.13 ± 0.01 U/L vs 0.24 ± 0.01 U/L,P < 0.01),and TNF-a levels(7.79 ± 2.35 pg/m L vs 10.87 ± 2.48 pg/m L,P < 0.05) in the intestinal tissue of rats.IP also markedly ameliorated the increase in ICAM-1(204.67 ± 53.27 vs 353.33 ± 45.19,P < 0.05) and VCAM-1(256.67 ± 58.59 vs 377.33 ± 41.42,P < 0.05) protein expression in the intestinal tissues.Additionally,IP remarkably decreased NF-κB activity(0.48 ± 0.16 vs 0.76 ± 0.22,P < 0.05) and protein expression(320.23 ± 38.16 vs 520.76 ± 40.53,P < 0.01) in rat intestinal tissue.CONCLUSION: IP may protect against IR-induced intestinal injury by attenuation of the neutrophilendothelial adhesion cascade via reducing ICAM-1 and VCAM-1 expression and TNF-a-induced NF-κB signaling pathway activity.
基金
Supported by Grants from the Fundamental Research Funds for the Central Universities,No.2013JDHZ08
Personnel training Specialized Research Fundation of The Second Affiliated Hospital of Xi’an Jiaotong University of China,No.RC(GG)201404
