PM2.5 Exposure Aggravates Oligomeric Amyloid Beta-induced Neuronal Injury Via NLRP3 Inflammasome

Background:The impact of air pollution on human health should not be ignored.Fine particulate matter(PM2.5)is a major atmospheric pollutant.Some studies have confirmed its role in respiratory and cardiovascular diseases.In recent years,more and more people believe that PM2.5 is also a potential risk factor for neurological diseases,especially neurodegenerative diseases.As the first major neurodegenerative disease,Alzheimer’s disease(AD)is still lack of effective drugs to delay the onset and progress of the disease.Therefore,it is more and more important to study the pathogenesis of ad in order to find effective methods of prevention and treatment.In this paper,the effects of PM2.5 on AD in vitro were studied,and a new idea for the prevention and treatment of ad was developed.Objective:To investigate the effect of PM2.5 on neurons and partial mechanism via NOD-like receptor pyrin domain containing 3(NLRP 3)inflammasome pathway in AD cell model.Materials and Methods:In this study,an invitro model of β amyloid oligomer(oAβ)stimulated neuron-microglia co-culture system was used as the research object.(1)To study the effect of PM2.5 on neurons in oAβ induced neuron-microglia co-culture system:LPS+oAβ(control group),LPS+oAβ+PM2.5(PM2.5 group),PM2.5 + Interleukin-1 receptor antagonist(PM2.5+IL-1ra group)were added to the neuron-microglial co-cultures,the apoptosis rate of each group was measured by flow cytometry,and the survival rate of each group was detected MTT assay.(2)To study the effect of PM2.5 on inflammation induced by oAβ in microglia cells:LPS+oAβ(control group),LPS+oAβ+PM2.5(PM2.5 group),PM2.5+caspase inhibitor/caspase-1 inhibitor(PM2.5+caspase inhibitor/caspase-1 inhibitor group)was added to microglia cultures,concentration of interleukin 1β(IL-1β)in supernatant of each group was mensurated by enzyme-linked immunosorbent assay(ELISA).Results:(1)Compared with the control group,the neuronal apoptosis rate increased and the neuronal survival rate decreased in the PM2.5 group,and the apoptosis rate and the neuronal survival rate increased in the PM2.5 IL-1ra group compared with the control group.(2)Compared with the control group,the IL-1β concentration in the microglia of the PM2.5 group increased.Compared with PM2.5 group,the concentration of IL-1β in microglia cells of PM2.5 caspase inhibitor/caspase-1 inhibitor group was decreased,and the concentration of IL-1β in microglia cells was in a concentration-dependent manner.Conclusion:PM2.5 aggravates the neuronal damage induced by oAβ by increasing IL-1β.PM2.5 activates caspase-1 to promote the secretion of il-1β by microglia.