AIM:To examine the effect of ganoderma lucidumpolysaccharide(GLP)on the immune liver injuryinduced by BCG infection,and investigate therelationship between degrees of hepatic damage andNO production in mice.METHODS:Immune hepatic injury was markedlyinduced by BCG-pretreatment(125 mg·kg~(-1),2-week,iv)or by BCG-pretreatment plus lipopolysaccharide(LPS,125 μg·kg~(-1),12-hour,iv)in mice in vivo.Hepatocellulardamage induced by BCG-pretreated plus inflammatorycytokines mixture(CM),which was included TNF-α,IL-1β,IFN-γ and LPS in culture medium in vitro.Administration of GLP was performed by oral orincubating with culture medium at immune stimulisimultaneity.Liver damage was determined by activityof alanine aminotransferase(ALT)in serum and inhepatocytes cultured supernatant,by liver weightchanges and histopathological examination.NOproduction in the cultured supernatant was determinedby the Griess reaction.Moreover,inducible nitric oxidesynthase(iNOS)protein expression was alsoexaminated by immunohistochemical method.RESULTS:Immune hepatic injury was markedly inducedby BCG or BCG plus inflammatory cytokines in BALB/cmice in vivoand in vitro.Under BCG-stimulated condition,augment of the liver weight and increase of the serum/supernatant ALT level were observed,as well asgranuloma forming and inflammatory cells soakage wereobserved by microscopic analysis within liver tissues.Moreover,NO production was also increased by BCG or/and CM stimuli in the culture supernatant,and a lot ofiNOS positive staining was observed in BCG-prestimulated hepatic sections.Application of GLPsignificantly mitigated hepatic tumefaction,decreasedALT enzyme release and NO production in serum/supernatant,improved the pathological changes ofchronic and acute inflammation induced by BCG-stimuliin mice.Moreover,the immunohistochemical resultshowed that GLP inhibited iNOS protein expression inBCG-immune hepatic damage model. CONCLUSION:The present study indicates that NOparticipates in immune liver injury induced byMycobacterium bovis BCG infection.The mechanismsof protective roles by GLP for BCG-induced immune liverinjury may be due to influence NO production in mice, AIM: To examine the effect of ganoderma lucidum polysaccharide (GLP) on the immune liver injuryinduced by BCG infection, and investigate therelationship between degrees of hepatic damage and NO production in mice. METHODS: Immune hepatic injury was markedly induced by BCG-pretreatment (125 mg·kg ~(-1),2-week,iv) or by BCG-pretreatment plus lipopolysaccharide(LPS,125 μg·kg -1 ,12-hour,iv)in mice in vivo.Hepatocellulardamageinduced by BCG-pretreated plus Inflammatory cytokines (CM), which was included TNF-α, IL-1β, IFN-γ and LPS in culture medium in vitro.Administration of GLP was performed by oral orincubating with culture medium at immune stimulisimultaneity.Liver damage was determined by activityof alanine The aminotransferase(ALT)in serum and inhepatocytes cultured supernatant,by liver weightchanges and histopathological examination.NOproduction in the cultured supernatant was determined by the Griess reaction.Moreover,inducible nitric oxidesynthase(iNOS)protein expression was alsoexaminat Ed by immunohistochemical method.RESULTS:Immune hepatic injury was markedly induced by BCG or BCG plus inflammatory cytokines in BALB/cmice in vivoand in vitro.Under BCG-stimulated condition,augment of the liver weight and increase of the serum/supernatant ALT level were observed. ,as well asgranuloma forming and inflammatory cells soakage wereobserved by microscopic analysis within liver tissues.Moreover,NO production was also increased by BCG or/and CM stimuli in the culture supernatant, and a lot ofiNOS positive staining was observed in BCG-prestimulated hepatic sections .Application of GLPsignificantly mitigated hepatic tumefaction,decreasedALT enzyme release and NO production in serum/supernatant,improved the pathological changes of chronic and acute inflammation induced by BCG-stimuliin mice.Moreover,the immunohistochemical resultshow how that GLP inhibited iNOS protein expression inBCG-immune hepatic damage Model. CONCLUSION: The present study indicates that NOparticipates in immune live r injUry induced by Mycobacterium bovis BCG infection.The mechanisms of protective roles by GLP for BCG-induced immune liver injury may be due to influence NO production in mice,