Anti-apoptotic Effect of Taxodione on Serum/Glucose Deprivation-Induced PC12 Cells Death

Abstract

Taxodione, a diterpenoid from the roots of Salvia chorassanica Bunge, possesses cytotoxic, apoptotic, and antimicrobial activity. This study was designed to investigate the protective effects of taxodione on serum/glucose deprivation-induced ischemic injury in PC12 cells and related mechanisms. In an in vitro model of ischemia, PC12 cells were exposed to serum and glucose deprivation for 6 and 18 h. The protective effects of the methanol extract of S. chorassanica and taxodione were assessed using alamarBlue(®) assay. Intracellular ROS production was measured by fluorimetry using 2',7'-dichlorofluorescin diacetate (DCFH-DA). The levels of PARP, Bcl-2, and Bax proteins were detected after western blot analysis. It was shown that taxodione (0.2-1.5 μM) significantly increased cell viability in a dose-dependent manner after ischemic insult. Taxodione has antioxidant activity and protects PC12 cells against oxidative stress-induced apoptotic cell death. Meanwhile, pretreatment with taxodione significantly induced an increase in Bcl-2 and a decrease in Bax protein level. The results of this study confirmed the protective effect of taxodione in serum/glucose deprivation-induced ischemic injury and the putative role of apoptosis as a underling mechanisms. Thus, it would be fair to consider taxodione as a promising ingredient of S. chorassanica for the expansion on novel class of anti-ischemic agents.

Synergistic and Defensive Properties of Emblica officinalis, Terminalia chebula, and Terminalia bellerica Extracts Against Serum/Glucose Deprivation-Induced PC12 Cells Death

“…Mousavi et al reported that intracellular ROS production significantly increased when PC12 cells were exposed to SGD condition (21). Other research also referred to the role of ROS production in SGD insult (25,26). In this study, SGD caused a major increase in ROS production that is in agreement with other reports.…”

Linalool attenuated ischemic injury in PC12 cells through inhibition of caspase‐3 and caspase‐9 during apoptosis

“…***p < .001 vs. control group, # p < .05, ## p < .01, ### p < .001 vs. OGD/R group. members which leads to activation of the mitochondria-dependent caspase signaling pathway (Mousavi et al, 2010;Shafaei-Bajestani et al, 2014). Bax over-expression can promote the apoptosis (Gao et al, 2016).…”

Repeated Glucose Deprivation/Reperfusion Induced PC-12 Cell Death through the Involvement of FOXO Transcription Factor

“…We modified the experimental conditions from previous reports for the reperfusion/hypoglycemic condition. The previous studies used oxygen-glucose deprivation for 4 hours/reperfusion for 20 hours [ 15 ]; serum and glucose deprivation for 6 and 18 hours [ 34 35 ]; and 2.5 hours oxygen-glucose deprivation, followed by a 24-hour reoxygenation period [ 36 ] to study PC-12 cell apoptosis. We used glucose deprivation for 1 hour/reperfusion for 23 hours and glucose deprivation for 6 hours/reperfusion for 18 hours, and continued for 5 days to evaluate the involvement of FOXO in repeated glucose deprivation/reperfusion, and compared them with the controls not exposed to hypoglycemia.…”