Luteolin is a common dietary flavonoid present in Chinese herbal medicines that 
has been reported to have important anti-inflammatory properties. Previous 
studies have shown that luteolin is an anti-inflammatory and anti-oxidative 
agent. In this study, the anti-virus inflammatory capacity of luteolin and its 
molecular mechanisms of action were analyzed. The cytotoxic effects of luteolin 
were assessed in the presence or absence of pseudorabies virus (PRV) via LDH and 
MTT assays. The results showed that luteolin (<10μM) had no toxic effects and 
there were tendencies toward higher cell survival. In PRV-infected RAW264.7 
cells, luteolin potently inhibited the production of NO, iNOS, COX-2 and 
inflammatory cytokine production. Luteolin did not inhibit the phosphorylation 
of ERK 1/2, p38, and JNK 1/2 either. We found that PRV-induced NF-κB activation 
is regulated through inhibition of STAT1and STAT3 phosphorylation in response to 
luteolin. Additionally, luteolin caused the induction of HO-1 via upregulation 
of Nrf2, both of which are involved in the secretion of proinflammatory 
mediators. The blockade of HO-1 expression with SnPP, a HO-1 inhibitor, 
attenuated HO-1 induction by luteolin and thus mitigated its anti-inflammatory 
effects during PRV-infected RAW264.7 cells. Taken together, our data indicate 
that luteolin diminishes the proinflammatory mediators NO, inflammatory 
cytokines and the expression of their regulatory genes, iNOS and COX-2, in 
PRV-infected RAW264.7 cells by inhibiting STAT1/3 dependent NF-κB activation and 
inducing Nrf2mediated HO-1 expression.