Background/Aims: Following injury to the liver, liver cells, including Kupffer cells and
hepatocytes express inducible nitric oxide synthase (iNOS), followed by the production of excess
levels of nitric oxide (NO). NO produced by iNOS has been found to contribute to liver injury. Treatment of primary
cultures of rat hepatocytes with the proinflammatory cytokine interleukin (IL)-1β stimulated iNOS expression and NO
production. Experiments with this in vitro hepatocyte model of liver injury and with in vivo animal models of liver injury
have demonstrated that drugs showing a liver-protective effect in vivo also inhibited the induction of iNOS expression and
NO production both in vivo and in vitro. Thus, in this in vitro hepatocyte model, the prevention of iNOS expression and
NO production are considered indicators of liver protection.
Results/Conclusion: This review describes a simple in vitro liver injury model, consisting of IL-1β-stimulated cultured
hepatocytes, and methods used to analyze the mechanisms of action of drugs that inhibit iNOS expression. This in vitro
hepatocyte model may be used to assess the liver-protective effects of pharmaceutical agents, herbal medicines, and
certain types of foods.