The Role Of Pro-/Anti-Inflammation Imbalance In A Beta 42 Accumulation Of Rat Brain Co-Exposed To Fine Particle Matter And Sulfur Dioxide

Taiyuan is a center of coal-based electricity production and many chemicals industries, where mixtures of sulfur dioxide (SO2) and particulate matter may be more prominent. The focus of the present study was to determine if there is a link between adverse effects in the brain and the combined-exposure to SO2 and fine particulate matter (PM2.5). Rats were exposed alternately to PM2.5 with different dosages (1.5, 6.0 and 24.0mg/kg body weight) and SO2 at the level of 5.6 mg/m(3). The results showed that the combined exposure to PM2.5 and SO2 enhanced the mRNA expression and protein level of TNF-a and IL-6 in rat cortex and hippocampus relative to the control, SO2 and PM2.5 alone. Instead, TGF-beta 1 mRNA and protein level were down-regulated in the brain. Additionally, PM2.5 at medium and/or high dose caused marked increase in A beta 42 level and PM2.5 thornSO(2) induced further increase of A beta 42 level in the cortex and hippocampus. It suggests that SO2 and PM2.5 can synergistically exert inflammation responses and induce A beta 42 accumulation in the brain. Also, it is notable that the A beta 42 accumulation of rat cortex and hippocampus were closely associated with pro-/anti-inflammatory cytokines ratio. These results clearly demonstrated that the combined exposure to PM2.5 and SO2 can induce the imbalance of pro-/anti-inflammatory cytokine, resulting in A beta 42 accumulation of rat brain cortex and hippocampus.