Effect of aminoguanidine on mitochondria injury from acute lung injury induced by LPS in rats
WU Hong-min
Abstract
WU Hong-min
Abstract
Aim The purpose of the present study was to examine the effect of selective inducible nitric oxide synthase (iNOS) inhibitor,aminoguanidine(AG),on mitochondria injury from acute lung injury induced by LPS in rats. Methods The rats were randomly devided into sham control group,LPS injury group and AG treatment group. The model of acute lung injury was prepared with injection of LPS in rat. AG was respec-tively administrated by intraperitioneal injection at 3 h after injury induced by LPS. Then rats were killed and the mitochondria of lungs was isolated by differential centrifugation. The activities of T-NOS, iNOS,ATPase,SOD and GSH-Px,and the contents of NO and MDA from mitochondria were respectively measured. Ultrastructure changes of lung mitochondria were examined by Electronic microscope after injury and AG treatment.Results The swelling of mitochondria was markedly increased,the activities of T-NOS and iNOS were significantly increased, the activities of ATPase,SOD and GSH-Px were significantly decreased,and the contents of NO and MDA were increased after acute lung injury.Compared with LPS group, administratition of AG significantly enhanced the activities of ATPase, SOD and GSH-Px,and decreased the contents of NO and MDA and the activity of iNOS in mitochondria. The study showed that lung cytoplasm and the mitochondria swelled, the cristae were disrupted, dissolved or disappeared after acute lung injury. AG could ameliorate these injury induced by LPS in rats. Conclusion AG could inhibit the production of NO,beneficially improve mitochondria energy pump, ameliorate oxidative injury, and effectively protected lung tissue against acute lung injury induced by LPS.
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Aim The purpose of the present study was to examine the effect of selective inducible nitric oxide synthase (iNOS) inhibitor,aminoguanidine(AG),on mitochondria injury from acute lung injury induced by LPS in rats. Methods The rats were randomly devided into sham control group,LPS injury group and AG treatment group. The model of acute lung injury was prepared with injection of LPS in rat. AG was respec-tively administrated by intraperitioneal injection at 3 h after injury induced by LPS. Then rats were killed and the mitochondria of lungs was isolated by differential centrifugation. The activities of T-NOS, iNOS,ATPase,SOD and GSH-Px,and the contents of NO and MDA from mitochondria were respectively measured. Ultrastructure changes of lung mitochondria were examined by Electronic microscope after injury and AG treatment.Results The swelling of mitochondria was markedly increased,the activities of T-NOS and iNOS were significantly increased, the activities of ATPase,SOD and GSH-Px were significantly decreased,and the contents of NO and MDA were increased after acute lung injury.Compared with LPS group, administratition of AG significantly enhanced the activities of ATPase, SOD and GSH-Px,and decreased the contents of NO and MDA and the activity of iNOS in mitochondria. The study showed that lung cytoplasm and the mitochondria swelled, the cristae were disrupted, dissolved or disappeared after acute lung injury. AG could ameliorate these injury induced by LPS in rats. Conclusion AG could inhibit the production of NO,beneficially improve mitochondria energy pump, ameliorate oxidative injury, and effectively protected lung tissue against acute lung injury induced by LPS.
Key concepts: Mitochondrion, Nitric oxide synthase, Nitric oxide, Chemistry, ATPase, Lung, Pharmacology, Superoxide dismutase