Sulforaphene Ameliorates Neuroinflammation and Hyperphosphorylated Tau Protein via Regulating the PI3K/Akt/GSK-3β Pathway in Experimental Models of Alzheimer’s Disease

Figure 13

The schematic drawing illustrating the action mechanisms underlying the effects of SF on ameliorating the cognitive impairments induced by STZ in rats. Our findings revealed that SF was able to suppress the activation of microglia and astrocytes to reduce the release of proinflammatory cytokines such as IL-6 and TNF-α, while promoting the production of the anti-inflammatory mediator such as IL-10. SF also inhibited tau protein phosphorylation by modulating the PI3K/Akt/GSK-3β pathway. Moreover, SF ameliorated neuroinflammation stimulated by LPS in BV-2 cells through inhibiting the NF-κB p65 translocation to the nucleus and regulating the PI3K/Akt/GSK-3β pathway. All these molecular actions of SF collectively contribute to its therapeutic effects on the experimental models of AD.