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KMID : 0358820050320030369
Journal of Korean Society of Plastic and Reconstructive Surgeons
2005 Volume.32 No. 3 p.369 ~ p.374
The Effect of Prostaglandin E©ûon Apoptosis Induced by Ischemia Reperfusion Injury in Rat Intestinal Mucosa
¹èÅÂÈñ/ Bae TH
±è½ÂÈ«/±èö±Ô/±èÇѱ¸/±è¿ì¼·/Kim SH/Kim CK/Kim HK/Kim WS
Abstract
Apoptosis is a physiologic or programmed cell death process which is controlled by genes. It is essential for the function and the appropriate development of multicellular organism. It is also thought to be one of the main mechanisms of cell death in ischemic tissues. The effect of prostaglandin E©û(PGE©û) is proven to be useful in the recovery of ischemic changes by inducing vasodilation of peripheral vessels and platelet disaggregation. PGE©ûis also known to suppress apoptosis in human liver sinusoidal endothelial cell from ischemia-reperfusion injury.
The purpose of this study is to evaluate the effects of PGE©ûon the apoptosis in the ischemia reperfusion injury of rat intestine.
Thirty Sprague-Dawley rats were used. In control group(N=15), superior mesenteric artery was occluded for 60 minutes and after removing the vessel clamp, it was reperfused for 60 minutes and harvested. In experimental group(N=15), a jejunal flap was also made as in the control group except for the intraarterial administration of the PGE©ûright after clamping the artery and removing the clamp.
H&E, TUNEL and immunohistochemical stains for p53, bax, and bcl-2 were performed. There were ischemic changes in gross and microscopic findings in both groups. The apoptotic index was significantly lower in the experimental group(1.29 ¡¾ 0.82(p=0.003)) than in the control group (2.33 ¡¾ 0.95). The rat intestinal ischemia apoptosis by ischemia-reperfusion was partly related to the modulating of bcl-2, bax, and p53 expression.
Our results indicate that PGE©ûsuppresses the apoptosis in the ischemic jejunal flap and this effect is probably the result of a increase in expression of bcl-2.
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