[PubMed] [Google Scholar] 19. AD-like pathologies were detected after multi-pullutants co-exposure. This work suggested PM2.5 plus FA co-exposure has more potential to induce AD-like pathologies than exposure alone. Oxidative stress and inflammation may be involved into the toxic mechanisms. Synergistic effects of co-exposure may induce the hygienic or safety standards of each pollutant not safe. valuevaluevaluevaluevaluevalueOD (MeanSD)value00.00104.001E?40.05020.0107PM2.50.00102.251E?40.87610.05380.01030.6035FA0.00114.907E?40.61010.05430.01000.5464FA+ PM2.50.01080.00480.0018(**)0.06330.00540.0405(*) Open in a separate window * em P /em 0.05, ** em P /em 0.01, compared with the control group. Glia activation in the mouse brain after PM2.5, FA or multi-pollutant treatment As Figure ?Figure5A5A & 5B shows, in the control animals the microglia display a ramified morphology with small cell bodies and elongated cell neurites, all characteristic features of resting microglia. After co-exposure, Iba1-positive cell size increases, neurites retract and coarsen, and some spines were found on the neurites. Significant changes in Iba1 levels were observed (Table ?(Table66). Open in a separate window Figure 5 Representative images (400) of the expression of Iba1 and GFAP as determined by immune-histochemical staining (brown color Dicer1 stain) and immunofluorescence(A) Expression of Iba1 (HIS). (B) Expression of Iba1 (IF, red). (C) Expression of GFAP (HIS). (D) Expression of GFAP (IF, red). Nuclei were stained by DAPI reagents (blue). Scale=50m. Through Figure ?Figure5C5C & 5D, astrocyte activation can also be observed. In vehicle animals, the astrocytes presented their normal morphology with non hypertrophic cell bodies and a ramified pattern of their branches. After co-exposure, astrocytes were activated, this activation was characterized by increased cell body volume and branches became more ramified. In addition, expression of fibrillary acidic protein (GFAP) in the cerebral cortex increased significantly (Table ?(Table6).6). However, PM2.5 or FA exposure alone did not induce microglia and astrocytes activation significantly. PM2.5, FA or multi-pollutant exposure exacerbates the oxidative stress (OS) and inflammation level in the mouse VU6001376 brain As Figure ?Figure66 shows, exposure to PM2.5 or FA alone had no or only minor adverse effects on the levels of OS in the mouse brain. But co-exposure exacerbated OS. Significant increases in reactive oxygen species (ROS) levels (Figure ?(Figure6A),6A), and a marked decrease in glutathione (GSH) content and superoxide dismutase (SOD) activity were seen after co-exposure (Figure ?(Figure6C6C & 6D). However, co-exposure not changed the levels of malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OH-dG). Open in a separate window Figure 6 The oxidative stress level after PM2.5, FA or multi-pollutant exposure(A) The relative fluorescence of ROS in the mouse brain after exposure. (B) The concentration of MDA in the mouse brain after exposure. (C) The concentration of GSH in the mouse brain after exposure. (D) The SOD activity in the mouse VU6001376 brain after exposure. (E) The level of 8-OH-dG in the mouse brain after exposure. * em P /em 0.05, ** em P /em 0.01, compared with the control group. The expression levels of nuclear VU6001376 factor B (NF-B), tumor necrosis factor (TNF-), interleukin-1 (IL-1), and Cyclooxygenase 2 (COX-2) were measured to reflect the inflammation level in the mouse brain (Figure ?(Figure7).7). PM2.5 or FA exposure alone did not change these cytokines expression. In the co-exposure group, the synergistic effect of co-exposure on COX-2 expression was significant. Open in a separate window Figure 7 The inflammation level after PM2.5, FA or multi-pollutant exposure(A) The concentration of NF-B in the mouse brain after exposure. (B) The concentration of TNF- in the mouse brain after exposure. (C) The concentration of IL-1 in the mouse brain after exposure. (D) The concentration of COX-2 in the mouse brain after exposure. * em P /em 0.05, ** em P /em 0.01, compared with the control group. DISCUSSION People usually consider that when we exposure to certain.