Prevents Increase of Hippocampal Tumor Necrosis Factor-α Independently of Its Effect on Brain-Derived Neurotrophic Factor in Rat Model of Chronic Stress.

ameliorates memory impairment and induces expression of hippocampal brain-derived neurotropic factor (BDNF) in chronically stressed rats. The relationship between the anti-inflammatory effect of on hippocampal BDNF and the involvement of sirtuin-1, a BDNF expression regulator, in neuroprotective mechanisms of warrants an investigation. We investigated the effect of ethanolic extracts (CA) on TNF-, IL-10, and SIRT1 levels and whether these predicted BDNF expression in rat hippocampus after chronic stress. For the experiments, thirty male rats () were divided into six groups: nonstressed-control, stressed-control, nonstressed +CA 300mg/kg/d, stressed +CA 150 mg/kg/d, stressed +CA 300 mg/kg/d, and stressed +CA 600 mg/kg/d. On day 28, rats were sacrificed and hippocampus was dissected out. Hippocampal TNF-, IL-10, SIRT1, and BDNF were measured by enzyme-linked immunosorbent assay. Hippocampal TNF- level was significantly higher in the stressed-control compared to nonstressed-control groups. Across all stress conditions, rats receiving the highest dose of CA had the lowest mean TNF- and highest mean BDNF. There were no significant differences in IL-10 and SIRT1 levels between groups. Hippocampal TNF- did not predict hippocampal BDNF in a regression analysis. In conclusion, lower TNF- and higher BDNF in the hippocampus support the hypothesis that these factors independently contribute to s neuroprotective effect in chronically stressed rats.