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2006•Acta Academiae Medicinae XuzhouRequires access

Bcl-2 and Bax participate in the protective role of endogenous nitric oxide in gastric ischemia/reperfusion injury of rat

Jianfu Zhang

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Abstract

Objective To investigate the effects of Bcl-2 and Bax on the protective role of endogenous nitric oxide(NO) in gastric ischemia/reperfusion(GI/R) injury of rat.?Methods The GI/R model was established by clamping the celiac artery for 30 min and allowing reperfusion for 3 h.The effects of L-arginine(L-arg,NO synthesis precursor) and L-NAME(NO synthesase blocker) on gastric mucosal cellular apoptosis,proliferation and Bcl-2 and Bax expression were investigated by using immunohistochemistry and Western blot in SD rats.?Results In the L-arg group,the gastric mucosal cellular injury induced by GI/R was significantly alleviated,showing decrease of apoptotic cells,increase of proliferative cells,increase of Bcl-2 expression and decrease of Bax expression,as compared with those in GI/R group(P0.05).In the L-NAME group,the results were the opposite: with the gastric mucosal cellular injury significantly aggravated and accompanied by increase of apoptotic cells,etc(P0.05).?Conclusion Bcl-2 and Bax participate in the protective role of endogenous nitric oxide in gastric ischemia/reperfusion injury of rat.

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Objective To investigate the effects of Bcl-2 and Bax on the protective role of endogenous nitric oxide(NO) in gastric ischemia/reperfusion(GI/R) injury of rat.?Methods The GI/R model was established by clamping the celiac artery for 30 min and allowing reperfusion for 3 h.The effects of L-arginine(L-arg,NO synthesis precursor) and L-NAME(NO synthesase blocker) on gastric mucosal cellular apoptosis,proliferation and Bcl-2 and Bax expression were investigated by using immunohistochemistry and Western blot in SD rats.?Results In the L-arg group,the gastric mucosal cellular injury induced by GI/R was significantly alleviated,showing decrease of apoptotic cells,increase of proliferative cells,increase of Bcl-2 expression and decrease of Bax expression,as compared with those in GI/R group(P0.05).In the L-NAME group,the results were the opposite: with the gastric mucosal cellular injury significantly aggravated and accompanied by increase of apoptotic cells,etc(P0.05).?Conclusion Bcl-2 and Bax participate in the protective role of endogenous nitric oxide in gastric ischemia/reperfusion injury of rat.

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Available abstract

Objective To investigate the effects of Bcl-2 and Bax on the protective role of endogenous nitric oxide(NO) in gastric ischemia/reperfusion(GI/R) injury of rat.?Methods The GI/R model was established by clamping the celiac artery for 30 min and allowing reperfusion for 3 h.The effects of L-arginine(L-arg,NO synthesis precursor) and L-NAME(NO synthesase blocker) on gastric mucosal cellular apoptosis,proliferation and Bcl-2 and Bax expression were investigated by using immunohistochemistry and Western blot in SD rats.?Results In the L-arg group,the gastric mucosal cellular injury induced by GI/R was significantly alleviated,showing decrease of apoptotic cells,increase of proliferative cells,increase of Bcl-2 expression and decrease of Bax expression,as compared with those in GI/R group(P0.05).In the L-NAME group,the results were the opposite: with the gastric mucosal cellular injury significantly aggravated and accompanied by increase of apoptotic cells,etc(P0.05).?Conclusion Bcl-2 and Bax participate in the protective role of endogenous nitric oxide in gastric ischemia/reperfusion injury of rat.

Key concepts: Nitric oxide, Apoptosis, Endogeny, Reperfusion injury, Ischemia, Immunohistochemistry, Pharmacology, Western blot

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