Tectorigenin attenuates the OGD/R-induced HT-22 cell damage through regulation of the PI3K/AKT and the PPARγ/NF-κB pathways. (August 2021)

• Record Type: Journal Article
• Authors: Yao, Li; Yang, Meili; Zhang, Juanli; Wang, Fei; Liu, Qing; Xie, Xiaojun; Liu, Zhuo; Guo, Qiang; Su, Hang; Zhai, Jiemin; He, Jianbo; Xue, Sha; Qiu, Zhengguo
• Is Part Of: Human & experimental toxicology. Volume 40:Number 8(2021)
• Page Start: 1320
• Page End: 1331
• Publication Date: 2021-08
• Subjects: Cerebral ischemia-reperfusion injury -- traditional Chinese medicine -- apoptosis -- ROS production -- inflammation; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327121993213
• Languages: English
• ISSNs: 0960-3271

Abstract

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-1β, IL-6, TNF-α production in OGD/R-induced HT-22 cells. Moreover, TEC activated PI3K/AKT signal pathway, increased PPARγ expression and inhibited NF-κB pathway activation in OGD/R-induced HT-22 cells. Further studies indicated that PPARγ inhibitor GW9662 activated NF-κB pathway after TEC treatment in OGD/R-induced HT-22 cells. Also, PI3K/AKT inhibitor LY294002, PPARγ inhibitor GW9662 and NF-κB 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 PPARγ/NF-κB pathways. These results indicated that TEC might be an effective compound in the treatment for ischemic brain injury.