4.3 Article

Tectorigenin attenuates the OGD/R-induced HT-22 cell damage through regulation of the PI3K/AKT and the PPARγ/NF-κB pathways

Journal

HUMAN & EXPERIMENTAL TOXICOLOGY
Volume 40, Issue 8, Pages 1320-1331

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1177/0960327121993213

Keywords

Cerebral ischemia-reperfusion injury; traditional Chinese medicine; apoptosis; ROS production; inflammation

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Tectorigenin (TEC) exhibits anti-inflammatory, anti-oxidant, and anti-apoptosis effects on oxygen-glucose deprivation/reperfusion (OGD/R)-induced HT-22 cells by activating the PI3K/AKT signal pathway, increasing PPARγ expression, and inhibiting NF-κB pathway activation. Furthermore, TEC may be a promising compound for the treatment of ischemic brain injury.
Tectorigenin (TEC) is an effective compound that derived from many plants, such as Iris unguicularis, Belamcanda chinensis and Pueraria thunbergiana Benth. Evidence suggested that TEC has anti-tumor, anti-oxidant activity, anti-bacterial and anti-inflammatory effects. In addition, there has some evidence indicated that TEC is a potential anti-stroke compound; however, its specific roles and associated mechanism have not yet been elucidated. In the present study, we aimed to investigate the anti-inflammatory, anti-oxidant activity and anti-apoptosis effects of TEC on oxygen-glucose deprivation/reperfusion (OGD/R)-induced HT-22 cells, and clarified the relevant mechanisms. Here, we observed that TEC significantly promoted cell survival, impeded cell apoptosis, inhibited ROS and inflammatory cytokines IL-1 beta, IL-6, TNF-alpha production in OGD/R-induced HT-22 cells. Moreover, TEC activated PI3K/AKT signal pathway, increased PPAR gamma expression and inhibited NF-kappa B pathway activation in OGD/R-induced HT-22 cells. Further studies indicated that PPAR gamma inhibitor GW9662 activated NF-kappa B pathway after TEC treatment in OGD/R-induced HT-22 cells. Also, PI3K/AKT inhibitor LY294002, PPAR gamma inhibitor GW9662 and NF-kappa B activator LPS both reversed the effects of TEC on OGD/R-induced HT-22 cell biology. Taken together, this research confirmed that TEC benefit to HT-22 cell survival and against OGD/R damage through the PI3K/AKT and PPAR gamma/NF-kappa B pathways. These results indicated that TEC might be an effective compound in the treatment for ischemic brain injury.

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