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Effect of aminoguanidine and L-arginine on mitochondria injury in acute lung injury rats induced by endotoxin

Shang Ta

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Abstract

Objective To investigate the effect of aminoguanidine and L-arginine(L-Arg)on mitochondria injury in acute lung injury rats induced by LPS.Methods The rats were randomly divided into control group,acute lung injury group,AG group(model group),AG+L-Arg group,and L-Arg group.The model of acute lung injury was prepared with injection of LPS in rats.Different drugs were respectively administrated through intraperitioneal injection 3 h after the injury induced by LPS,and rats were killed and the mitochondria of lungs was isolated by differential speed centrifugation.The activities of T-NOS,iNOS,ATPase,SOD and GSH-Px,the contents of NO and MDA in mitochondria were respectively measured.Results The activities of T-NOS and iNOS were significantly increased(P0.05 or0.01),the activities of ATPase,SOD and GSH-Px were significantly decreased too(P0.05 or0.01),and the contents of NO and MDA were increased after acute lung injury(P0.05 or0.01).Conclusion Aminoguanidine and L-arginine can inhibit effectively the activity of iNOS,enhance the activity of eNOS,improve mitochondria energy pump,change the production of NO,relieve oxidative injury,so that which can effectively protect lung tissue against acute lung injury induced by LPS.

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Objective To investigate the effect of aminoguanidine and L-arginine(L-Arg)on mitochondria injury in acute lung injury rats induced by LPS.Methods The rats were randomly divided into control group,acute lung injury group,AG group(model group),AG+L-Arg group,and L-Arg group.The model of acute lung injury was prepared with injection of LPS in rats.Different drugs were respectively administrated through intraperitioneal injection 3 h after the injury induced by LPS,and rats were killed and the mitochondria of lungs was isolated by differential speed centrifugation.The activities of T-NOS,iNOS,ATPase,SOD and GSH-Px,the contents of NO and MDA in mitochondria were respectively measured.Results The activities of T-NOS and iNOS were significantly increased(P0.05 or0.01),the activities of ATPase,SOD and GSH-Px were significantly decreased too(P0.05 or0.01),and the contents of NO and MDA were increased after acute lung injury(P0.05 or0.01).Conclusion Aminoguanidine and L-arginine can inhibit effectively the activity of iNOS,enhance the activity of eNOS,improve mitochondria energy pump,change the production of NO,relieve oxidative injury,so that which can effectively protect lung tissue against acute lung injury induced by LPS.

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Available abstract

Objective To investigate the effect of aminoguanidine and L-arginine(L-Arg)on mitochondria injury in acute lung injury rats induced by LPS.Methods The rats were randomly divided into control group,acute lung injury group,AG group(model group),AG+L-Arg group,and L-Arg group.The model of acute lung injury was prepared with injection of LPS in rats.Different drugs were respectively administrated through intraperitioneal injection 3 h after the injury induced by LPS,and rats were killed and the mitochondria of lungs was isolated by differential speed centrifugation.The activities of T-NOS,iNOS,ATPase,SOD and GSH-Px,the contents of NO and MDA in mitochondria were respectively measured.Results The activities of T-NOS and iNOS were significantly increased(P0.05 or0.01),the activities of ATPase,SOD and GSH-Px were significantly decreased too(P0.05 or0.01),and the contents of NO and MDA were increased after acute lung injury(P0.05 or0.01).Conclusion Aminoguanidine and L-arginine can inhibit effectively the activity of iNOS,enhance the activity of eNOS,improve mitochondria energy pump,change the production of NO,relieve oxidative injury,so that which can effectively protect lung tissue against acute lung injury induced by LPS.

Key concepts: Medicine, Lung, Mitochondrion, Arginine, Nitric oxide, Pharmacology, Anesthesia, Internal medicine

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Effect of aminoguanidine and L-arginine on mitochondria injury in acute lung injury rats induced by endotoxin — Research Paper | ScholarLens