Research On The Association Between IL-32and Alzheimer’s Disease

【Objecfive】 To discuss the expression level of interleukin-32(IL-32) in gliomawhile treated with Aβand through analysis the relationship of IL-32and TNF-α inorder to take its inflammation’s regulatory mechanism in alzheimer’s disease.【Methods】 Deal U251with Serum starvation in order to unified their’s growthcondition and then stimulued with different concentrations of Aβ42(0ug/ml,5ug/ml,10ug/ml,20ug/ml and30ug/ml,40ug/ml), each group detected with MTS to selecthalf survival rate concentration for the follow-up experiments.Then,half survival rateconcentration Aβ dealing with U2510h,6h,12h and24h. Collect cells total RNA andreverse into cDNA and RT-PCR was employed to detect the mRNA expression ofIL-32and TNF-α；Collect cell total protein and western blot was employed to detectthe protein expression of IL-32and TNF-α.【Results】 Compared with control group, Real-time PCR detection showed thatIL-32and TNF-α mRNA expression were remarkable improved while deal with30ug/ml Aβin different time (6h,12h and24h), the change were noted (P <0.01).Compared with TNF-α, IL-32mRNA expression is more in every group (P <0.01),and the change of IL-32mRNA expression were more outstanding while dealed withAβ(P <0.01). Western blot showed that IL-32protein expression is less than TNF-αin every group (P <0.01),30ug/ml Aβ stimulated U251with different time (6h,12hand24h) show that Aβ can promote IL-32protein expression levels (6h: P <0.05;12hand24h: P <0.01, with control group)；And so it is TNF-α（6h:P＜0.05，12h和24h:P＜0.01）. Pearson correlation analysis of the mRNA and protein expression of IL-32and TNF-α showed that different time and the same concentration of Aβ treatmentgroups IL-32and TNF-α was significantly positively related to each other, the rusultswere noted (mRNA:r=0.965, P <0.001，protein: r=0.946, P <0.001).【Conclusions】1. IL-32may participate in alzheimer’s disease progression mechanism of immune inflammation;2. In a way, The long human have AD，thehigher IL-32expression in their brain;3.The expression of IL-32were significantlycorrelated with the expression of TNF-α, IL-32as a kind of inflammation factor mayinduce the production of TNF-α, and IL-32partly based on the expressions of TNF-α;4.The protein expression of IL-32in brain may only in a certain subtype.