Fig. 4: Inhibition of NMDAR ameliorates Erastin- or RSL3-induced ferroptosis in vitro.
From: NMDARs activation regulates endothelial ferroptosis via the PP2A-AMPK-HMGB1 axis
A Glutamate release in HUVECs treated with Erastin in the presence of the NMDAR inhibitor MK801. B MTT assay showing HUVECs treated with Erastin or RSL3 in the presence of MK-801. C Ultrastructure of mitochondria in HUVECs treated with Erastin or RSL3 in the presence of MK-801. Black arrowheads: shrunken mitochondria. Scale bars, 5 μm. D GSH content in HUVECs pretreated with ferroptosis inducers (Erastin, 10 μM; RSL3, μM) for 24 h and then treated with MK801. E Representative flow cytometry image and quantification (F) of LOS production in HUVECs pretreated with a ferroptosis inducer (Erastin, 10 μM; RSL3, μM) for 24 h and treated with MK801. G Immunoblots and quantification (H) of SLC7A11, GPX4, p-PP2A, PP2A, p-AMPK, AMPK, and HMGB1 in HUVECs pretreated with a ferroptosis inducer (Erastin, 10 μM; RSL3, μM) for 24 h and treated with MK801. I Scheme of the protective mechanism of inhibiting HMGB1 overexpression by MK-801 treatment against ferroptosis in VECs. **P < 0.01 and ***P < 0.001 vs control; #P < 0.05, ##P < 0.01 and ###P < 0.001 vs Erastin; &P < 0.05 and &&P < 0.01 vs RSL3.
