Effects of gastric ischemia-reperfusion on gastric mucosal cellular apoptosis and proliferation in rats.
The effect of gastric ischemia-reperfusion (GI-R) on gastric mucosal cellular apoptosis and proliferation was investigated using histological, immunohistochemical methods in Sprague-Dawley rats. The GI-R model was established by clamping the celiac artery for 30 min and reperfusing for 0, 0.5, 1, 3, 6, 24, 48, 72 h, respectively. Mild gastric mucosal injury was induced by ischemia alone. However, the injury worsened and reached the maximum at 1 h after reperfusion, almost simultaneously with the gastric mucosal cellular apoptosis increase and cellular proliferation decrease in gastric mucosa. Then, gastric mucosal cells began to repair by increasing gastric cellular proliferation, which achieved the maximum at 24 h after reperfusion. The mucosal lesions were almost completely repaired at about 72 h after reperfusion. These results indicate that the gastric mucosal injury after GI-R is mainly induced by reperfusion. The damaged gastric mucosa could initiate its repairing mechanism immediately through inhibiting cellular apoptosis and increasing the number of proliferative cells, which substitute the damaged cells gradually. The plerosis almost completes in three days after reperfusion showing a strong self-repair ability of gastric mucosa.
Qiao
Wei-Li
WL
Department of Physiology, Xuzhou Medical College, Xuzhou 221002, China.
Wang
Lin
L
Zhang
Jian-Fu
JF
Zhang
Yong-Mei
YM
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D049109:Cell Proliferation; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology* / Q000502:physiology; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000502:physiology; D015427:Reperfusion Injury / Q000503:physiopathology*; D013270:Stomach / Q000098:blood supply / Q000473:pathology / Q000502:physiology