Effect Of Ginsenoside Rg1, Rh2 On The Expression Of IL-1β, INOS And TNF-α In Activated Microglia By Aβ

【Objectives】To investigate the expression of the genes encoding IL-1βand iNOS in a murine microglia cell line BV-2 activated by Aβ,and to study the effect of ginsenoside Rg1 and Rh2 on the modulation of the cytokine expression in these experimental steps,so as to provide basis for the pathogenesis and anti-inflammatory treatment of AD in vitro.【Methods】Microglia cell line BV-2 activated by Aβin presence or absence of various concentration of ginsenoside Rgl and Rh2,cell morphology was observated,cell viability was assayed by MTT assay,IL-1βand iNOS mRNA expression was detected by RT-PCR and the protein expression of TNF-αwas measured by immunocytochemistry.The data were expressed by mean±std and analysed statistically by SPSS11.5.【Results】At the doses and effect time studied,Aβ(0～30μmol/L,＜36h),Rg1 and Rh2 had no toxicity in BV-2 cells respectively.Aβ(15μmol/L)in combination with Rg1(≤40μmol/L)or Rh2(≤20μmol/L)also had no toxicity.The expression of IL-1βmRNA was induced by Aβin a dose dependent manner,but not iNOS.The expression of the IL-1βhad a peak time and significantly decreased at 24h,but the peak time of iNOS was later than IL-1β,the expression of which was relatively stable within 12-24h.When Rg1 and Rh2 were intervened BV-2 activated by Aβ,the expression of IL-1βand iNOS mRNA and TNF-αwas significantly decreased.【Conclusions】Aβcould stimulate the expression of IL-1βand iNOS mRNA,then enlarge the cascaded inflammatory reaction,which has been thought to be associated with the onset of AD.Ginsenoside Rg1 and Rh2 could decrease the expression of IL-1β,iNOS and TNF-α,alleviate the inflammatory reaction,furthermore inhibit oxide stress,and thus reduce the injury of neurons.Rg1 and Rh2 has protective action in the pathogenesis of AD and this effect meffectassociated with its antioxidation and anti-inflammatory activity.