Tenuifoliside A inhibits corticosterone-induced neurotoxicity of rat glioma cells via ERK pathway

Aim: To investigate the neuroprotective effects of Tenuifoliside A (TFSA) on corticosterone-induced injury in rat glioma cells and explore the potential mechanism. Methods: The injury model was established by treating C6 cells with 0.8 mmol·L^-1 of corticosterone (CORT) by 48h; C6 cells were pretreated with CORT for 30 min followed by co-treated with 30, 10 and 3 μmol·L^-1 of TFSA for 48 h. Cell viability was detemined by Cell Counting Kit (CCK) assay; Hoechst 33258 staining was used to identify the neuroprotective effects of TFSA against neurotoxicity induced by CORT; Western blot was used to detect the expression of ERK, Bcl-2 and Bax protein. Caspase-3 activity was as a specific apoptotic marker in C6 cells exposed to CORT alone or co-treated with TFSA was also assayed. Results: Compared with normal control group, CORT significantly decreased the viablity of C6 cells to 69.58% (P < 0.01). Western blot results showed that the protein levels of ERK and Bcl-2 decreased significantly. In contrast, the expression of Bax and the activity of Caspase-3 increased markedly (P < 0.01). However, TFSA could increase the viability of C6 cells damaged by CORT up to 84.48% (P < 0.01). Moreover, TFSA increased the protein level of ERK, Bcl-2 and decreased the protein level of Bax and the activity of Caspase-3 in C6 cells exposed to CORT(P < 0.01). Conclusion: TFSA protects C6 cells from CORT-induced damage, and the neuroprotective mechanism may be associated with the activation of Bcl-2 and suppressing Bax and the activity of Caspase-3 via ERK pathway.