Inhibitive Effect of Resveratrol on the Inflammation in Cultured Astrocytes and Microglia Induced by Aβ1-42

Astrocytes and microglia appear central to the initiation and progression of neuroinflammation in Alzheimer's disease (AD). In this study, inflammation was mimicked by Aβ1-42 treatment of rat astrocytes (RA) and N9 microglia cell lines. Inflammation induced by Aβ1-42 can be inhibited by pyrrolidine dithiocarbamic acid (PDTC), indicating that the NF-κB signal pathway is involved in inflammation. Then, the inhibitive effects of resveratrol (Res) on the inflammation in RA and N9 cells were assessed by observing the changes in inflammatory factors, chemokines, cell cycle and adhesion molecules on the cell surface. 17β-Estradiol was used as an estrogen-positive control because Res is one of the selective estrogen receptor modulators. In RA cells, TNF-α, IL-1β and MCP-1 in the supernatant and the proliferation index in the cell cycle were decreased by 5, 12.5, and 25 μM Res and 20 nM 17β-estradiol treatment 24 h before Aβ1-42. Similarly, in N9 microglial, the levels of IL-1β, IL-6 and NO in the supernatant and CD40 and MHCII in the 10, 20, and 40 μM Res and 20 nM 17β-estradiol treatment groups decreased markedly compared with the Aβ1-42 treatment group. In addition, Res decreased the nuclear translocation of NF-κB/p65 when checked by immunofluorescence. Furthermore, Res increased the expression of NF-κB/p65 and decreased the expression of p-IκB in the cytoplasm in both RA and N9 microglia. Taken together, the present data indicate that Res reduces inflammation in RA and N9 microglia, and the anti-NF-κB signal pathway may be one of the target mechanisms.