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. 2019 Jun 7;10:638. doi: 10.3389/fphar.2019.00638

Figure 2.

Figure 2

Baicalein attenuates FAC-induced neuronal damage by inhibiting ferroptosis. (A) Cell viability was measured with CCK8 assay, in which HT22 cells were incubated with various concentrations (37.5, 75, 150, and 300 μM) of FAC for different periods of time (12–36 h). (B) HT22 cells were incubated with different concentrations (1, 2, 4, 8, 16, and 32 μM) of baicalein for 2 h, prior to incubation with 300 μM of FAC for 36 h. (C) FAC exposure caused cell shrinkage and nuclear condensation. Baicalein pretreatment reduced cell death. Scale bar: 200 μm (D) after 2 h pretreatment with 32 μM baicalein, 12.5 μM Fer-1, and 1 μM Lipo-1, lipid ROS in HT22 cells was assessed by FACS analysis of C11-BODIPY fluorescence after treatment with FAC for 36 h. (E) Representative Western blots of 4-HNE with 32 μM baicalein and ferroptosis inhibitors pretreatment for 2 h in the FAC-induced HT22 cell injury model. (F) The relative mRNA expression of PTGS2 was reduced after baicalein and ferroptosis inhibitors pretreatment. (G) Representative Western blots of GPX4 with 32 μM baicalein and ferroptosis inhibitors pretreatment for 2 h in the FAC-induced HT22 cell injury model. Data are representative of three independent experiments with similar results, *p < 0.05, **p < 0.01, and ***p < 0.001.