Modulation of no synthesis by plaferon LB in liver

Nitric oxide (NO) is a free radical involved in the regulation of many physiological processes. NO exerts important effects on liver in health and diseases. In the present study, we attempted to evaluate the influence of plaferon LB on the liver injury in two experimental models: immune-mediated and mechanical (traumatic shock) liver damage models. The results of our study demonstrated that plaferon LB decreased levels of NO in traumatic shock, but enhanced NO expression on con-A induced hepatitis. Furthermore, plaferon LB inhibited development of metabolic changes in liver tissue and facilitated restoration of hepatocyte function and structure of the tissue. Thus, our data revealed that plaferon LB was a powerful regulator of NO levels in experimental liver injury. Further investigations are needed to determine pro- and anti-apoptotic properties of plaferon LB in the liver.