Fig. 6.

Protective effects of FCPR03 in ameliorating ER stress and reducing apoptosis are abolished by ML385. (A, C, E) HT-22 cells pre-treated with the Nrf-2 inhibitor ML385 (5 μM), were treated with FCPR03 (20 μM) for 1 h followed by 6 h of OGD. The protein levels of GRP78, p-eIF2α, eIF2α, and CHOP were determined by Western blotting. (B, D, F) The relative protein levels of GRP78/β-tubulin (n = 4), p-eIF2α/eIF2α (n = 3) and CHOP/β-tubulin (n = 4) were measured by semiquantitative analysis of the Western blots. (G) HT-22 cells pre-treated with the Nrf-2 inhibitor, ML385, were treated with FCPR03 for 1 h followed by OGD for 6 h and re-oxygenation for 24 h, and then the cell viability was detected by a CCK-8 assay (12 duplications from three independent experiment, n = 3). (H, I) HT-22 cells were processed as described above, and the variation of cleaved-caspase 3 was determined by Western blotting. The relative level of cleaved-caspase 3/pro-caspase 3 was measured by semiquantitative analysis of the Western blots (n = 4). Results are expressed as the mean ± SD, *P < 0.05, **P < 0.01 versus the indicated group.