Nitric oxide can also cross biological membranes and travel significant distances in cells and non-small-cell lung carcinoma tissues. Lang et al recently reported that inhaled NO accelerates restoration of liver function in adults following liver transplantation. It has also been reported that IPO could stimulate production of NO, so we deter mined if IPO would protect liver against liver I/R injury through NO mediated production. We observed the changes of NO levels in serum and tissues, as well as NOS. Until now, three different kinds of NOS have been identified. Previous study has demonstrated that nNOS were expressed in liver tissue of mouse, but it has been reported that nNOS is mainly involved in neu ronal signaling and it does not participate in the events involved during I/R.

So we detected the serum levels of NO, TNOS, eNOS, iNOS Inhibitors,Modulators,Libraries and production of TNOS, eNOS, iNOS in liver tissues. Hepatic I/R significantly reduced both the serum levels of NO, TNOS, eNOS, iNOS and production of TNOS, eNOS, iNOS in liver tissues. Increased NO, eNOS in serum and eNOS in tissue were found in IPO I/R group, while no significant differences were found in TNOS and iNOS in serum and tissues between I/R and IPO I/R group. L NAME decreased the serum levels of NO, TNOS, eNOS and iNOS, pro duction of TNOS, eNOS, iNOS in liver tissues. eNOS was reported to play a beneficial role against I/R injury. It was found that eNOS could lead to amelioration of I/ R induced liver injury and protect Inhibitors,Modulators,Libraries against renal I/R injury. eNOS over expression also could lead to reduced infarct sizes after cardiac I/R injury.

NO production by eNOS seems to be of central importance in ischemic injury. It has been reported that eNOS derived NO production constitutes a promising therapeutic approach to prevent myocardial I/R injury. Our results showed that increased eNOS levels both in serum and tissue using assay kits. So it increased both locally and systemically, and that might Inhibitors,Modulators,Libraries contribute to NO production and liver protection. These findings support our hypothesis that the IPO elevates NO and eNOS levels, which in turn reduces or compensates the I/R induced hepatic injury. ROS play a critical role in the I/R injury. After warm ischemia, ROS were produced at the moment of reper fusion and promoted the adhesion of leukocytes to microvascular endothelium.

Our study showed that IPO post treatment reversed the increase of MDA levels to a considerable Inhibitors,Modulators,Libraries extent, thereby confirming its antioxi dant role in I/R. Furthermore, we showed that SOD activity significantly increased in IPO I/R group. Inhibitors,Modulators,Libraries Total SOD activity is decreased following I/R injury, and the decrease would render the tissue susceptible to oxi dant injury. Therefore, the elevated SOD activity induced by IPO post treatment may contribute to reduce superoxide radicals following liver I/R. Our results indicated IPO may reduce the oxidative stress caused by hepatic warm I/R injury and attenuate subse quent organ nothing damages.