Fig. 2: Protective effects of MK801 against LPS-induced mitochondrial dysfunction in HUVECs. | Cell Death Discovery

Fig. 2: Protective effects of MK801 against LPS-induced mitochondrial dysfunction in HUVECs.

From: NMDARs antagonist MK801 suppresses LPS-induced apoptosis and mitochondrial dysfunction by regulating subunits of NMDARs via the CaM/CaMKII/ERK pathway

Fig. 2

A Flow cytometry graphs and B analysis of mitochondrial transmembrane potential in HUVECs treated with LPS in the absence or presence of indicated doses of MK801. Representative of traces (C) and quantification at 10 min (D) of mitochondria Ca2+ influx labeled with Rhod-2 AM in HUVECs treated with LPS in the presence or absence of Ru360 (mitochondrial calcium uptake inhibitor), DS16570511 (MCU inhibitor), or MK801 for 2 h. E–H O2 consumption rates (D), basal (E) and maximal respiration rate (F), and ATP production (G) in HUVECs treated with LPS in the presence or absence of MK801. Representative of western blotting images (I) and quantification (J) of NDUFB8, SDHB2, UQCRC2, MTCO1, and ATP5a in HUVECs treated with LPS in the presence or absence of MK-801 at indicated doses. (Data are presented as mean ± SEM, ***P < 0.001, **P < 0.01, *P < 0.05 vs. Control; ###P < 0.001, ##P < 0.01, #P < 0.05 vs. LPS).

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