Interaction between HO-1/CO and iNOS/NO in acute lung injury induced by intestinal ischemia-reperfusion in rats
Ouyang Jing-pin
Abstract
Ouyang Jing-pin
Abstract
Objective To observe the interaction between HO-1/CO and iNOS/NO in acute lung injury induced by intestinal ischemia-reperfusion in rats.Methods Thirty-two Wistar rats,weighed 200~250 g were randomly divided into four groups with 8 animals in each group: sham-operation group,I/R group in which intestinal I/R was produced by clamping super mesenteric artery(SMA) for 1 hour and declamping SMA for 6 hours,AG group and Hemin group.MDA content in lung,the concentrations of CO in artery and the activities of serum NO were observed in the rat models of acute lung injury induced by intestinal ischemia-reperfusion.HO-1's and iNOS's expressions in rat lung tissue were detected by immunohistochemistry and morphometry computer image analysis.The histological changes of lung were observed under light microscope.Results Compared with sham group,HO-1's and iNOS's expressions were markedly increased in I/R group(P0.01).But in AG group,HO-1's and iNOS's expressions were significantly lower than those in I/R group;in hemin group,expression of HO-1 was obviously higher while iNOS was significantly lower than that in I/R group(P0.05).The concentrations of CO,content of MDA and the activity of serum NO in I/R group were significantly higher than those in sham group(P0.05 or P0.01). The concentrations of CO was obviously higher in Hemin group,but was significantly lower in AG group(P0.05 or P0.01).Under light microscope,the pathological changes induced by I/R were significantly attenuated by AG and Hemin.Conclusion Both CO and NO play a role in lung protection in intestinal ischemia-reperfusion.There is interaction between them.CO may in fluence iNOS/NO by way of HO-1 and inducement of iNOS may influence HO/CO.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To observe the interaction between HO-1/CO and iNOS/NO in acute lung injury induced by intestinal ischemia-reperfusion in rats.Methods Thirty-two Wistar rats,weighed 200~250 g were randomly divided into four groups with 8 animals in each group: sham-operation group,I/R group in which intestinal I/R was produced by clamping super mesenteric artery(SMA) for 1 hour and declamping SMA for 6 hours,AG group and Hemin group.MDA content in lung,the concentrations of CO in artery and the activities of serum NO were observed in the rat models of acute lung injury induced by intestinal ischemia-reperfusion.HO-1's and iNOS's expressions in rat lung tissue were detected by immunohistochemistry and morphometry computer image analysis.The histological changes of lung were observed under light microscope.Results Compared with sham group,HO-1's and iNOS's expressions were markedly increased in I/R group(P0.01).But in AG group,HO-1's and iNOS's expressions were significantly lower than those in I/R group;in hemin group,expression of HO-1 was obviously higher while iNOS was significantly lower than that in I/R group(P0.05).The concentrations of CO,content of MDA and the activity of serum NO in I/R group were significantly higher than those in sham group(P0.05 or P0.01). The concentrations of CO was obviously higher in Hemin group,but was significantly lower in AG group(P0.05 or P0.01).Under light microscope,the pathological changes induced by I/R were significantly attenuated by AG and Hemin.Conclusion Both CO and NO play a role in lung protection in intestinal ischemia-reperfusion.There is interaction between them.CO may in fluence iNOS/NO by way of HO-1 and inducement of iNOS may influence HO/CO.
Key concepts: Hemin, Medicine, Superior mesenteric artery, Lung, Reperfusion injury, Internal medicine, Ischemia, Intestinal ischemia