The Effect of Prostaglandin E1 on Apoptosis Induced by Ischemia Reperfusion Injury in Rat Intestinal Mucosa.
- Author:
Tae Hui BAE
1
;
Seung Hong KIM
;
Cheol Kyu KIM
;
Han Koo KIM
;
Woo Seob KIM
Author Information
1. Department of Plastic and Reconstructive Surgery, College of Medicine, Chung-Ang University, Seoul, Korea. shkimps@ lycos.co.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Prostaglandin E1;
Intestines;
Ischemia- reperfusion injury
- MeSH:
Alprostadil*;
Animals;
Apoptosis*;
Arteries;
Blood Platelets;
Cell Death;
Coloring Agents;
Constriction;
Endothelial Cells;
Humans;
In Situ Nick-End Labeling;
Intestinal Mucosa*;
Intestines;
Ischemia*;
Liver;
Mesenteric Artery, Superior;
Rats*;
Rats, Sprague-Dawley;
Reperfusion Injury*;
Vasodilation
- From:Journal of the Korean Society of Plastic and Reconstructive Surgeons
2005;32(3):369-374
- CountryRepublic of Korea
- Language:Korean
-
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 E1(PGE1) is proven to be useful in the recovery of ischemic changes by inducing vasodilation of peripheral vessels and platelet disaggregation. PGE1 is 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 PGE1 on 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 PGE1 right 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+/-0.82(p=0.003)) than in the control group (2.33+/-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 PGE1 suppresses the apoptosis in the ischemic jejunal flap and this effect is probably the result of a increase in expression of bcl-2.
