Oxidative Medicine and Cellular Longevity / 2019 / Article / Tab 3

Review Article

The Nrf2/HO-1 Axis as Targets for Flavanones: Neuroprotection by Pinocembrin, Naringenin, and Eriodictyol

Table 3

Neuroprotective effect of flavanones through the Nrf2/HO-1 mechanism: eriodictyol.

CompoundExperimental modelKey findingsReference

EriodictyolAβ25-35 peptide-induced oxidative cell death in primary cortical neurons (20, 40, and 80 μM)Attenuates the induced apoptosis and activation of c-Jun N-terminal kinases (JNK)/p38 signaling pathway; increases Nrf2 protein levels and subsequent activation of ARE pathway genes in primary cultured neurons—protective effects attenuated by RNA interference-mediated knockdown of Nrf2 expression.Jing et al. [67]

Eriodictyol-7-O-glucosideCultured primary astrocytes—oxygen and glucose deprivation-induced oxidative insult; rat model of focal cerebral ischemiaProtects against the induced cell death; increases the nuclear localization of Nrf2 and induces the expression of the Nrf2/ARE-dependent genes—protective effect abolished by RNA interference-mediated knockdown of Nrf2 expression; reduces the amount of brain damage and ameliorates neurological deficits in vivo.Jing et al. [68]

EriodictyolCultured rat pheochromocytoma (PC12) cells exposed to H2O2-induced neurotoxicity (20, 40, and 80 μM)Inhibits apoptosis; induces the nuclear translocation of Nrf2, enhances the expression of HO-1 and γ-GCS, and increases the levels of intracellular GSH—Nrf2 small interference RNA abolished the induced HO-1 and γ-GCS expression and cytoprotective protective effects.Lou et al. [69]

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