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Chemical agents | Models | Involved mechanisms | Effect | Reference |
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Resveratrol | Rat astrocytes induced by amyloid-beta (Aβ) | Upregulation of SIRT1 decreases the nuclear translocation of NF-κB p65 | Suppression of inflammatory cytokines (TNF-α, IL-1β, and MCP-1) | Zhao et al. [101] |
Resveratrol | N9 microglia cell lines induced by amyloid-beta (Aβ) | Upregulation of SITRT1 decreases the nuclear translocation of NF-κB p65 | Suppression of inflammatory cytokines (IL-1β, IL-6, and NO) | Zhao et al. [101] |
Resveratrol | Primary glial from rat cortices induced by amyloid-beta (Aβ) | Upregulation of SIRT1 inhibits NF-κB p65 by deacetylating Lys310 residue | Suppression of iNOS and EGFP expression; improvement of the survival of MAP2-positive neurons | Chen et al. [102] |
Resveratrol | Cerebral ischemia mouse model; primary cortical neurons induced by oxygen-glucose deprivation (OGD) | The high levels of acetylation of NF-κB p65 occur in mouse and cell models; resveratrol deacetylated the Lys310 in primary neurons after OGD | Suppression of LDH expression and improvement of the survival of neuronal cell | Lanzillotta et al. [103] |
Resveratrol | Postoperative cognitive dysfunction (POCD) rat model | Upregulation of SIRT1 decreases the expression of acetyl-NF-κB p65 in the hippocampus | Suppression of inflammatory cytokines (TNF-α, IL-1β, and IL-6) | Yan et al. [73] |
Resveratrol | LPS-induced depressive-like behaviors mouse model | Upregulation of SIRT1 decreases the expression of NF-κB in the hippocampus | Suppression of LPS-induced depression-like behaviors and the overactivation of microglia | Liu et al. [104] |
Resveratrol | Alzheimer’s disease rat model induced by ovariectomized (OVX)+D-galactose (D-gal) | Upregulation of SITRT1 decreases the expression of NF-κB p65 in the hippocampus | Suppression of insoluble amyloid-beta (Aβ) and MMP-9; increase of the tight junction protein claudin-5 | Zhao et al. [105] |
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