Fig. 5: mPGES-2 accelerates mitochondrial oxidative stress, lipid peroxidation, and ferroptosis in HK-2 cells induced by cisplatin. | Cell Death & Disease

Fig. 5: mPGES-2 accelerates mitochondrial oxidative stress, lipid peroxidation, and ferroptosis in HK-2 cells induced by cisplatin.

From: Targeting mPGES-2 to protect against acute kidney injury via inhibition of ferroptosis dependent on p53

Fig. 5

mPGES-2 overexpressing HK-2 cells were generated and exposed to 20 μM cisplatin for 24 h to mimic AKI in vivo. A BODIPY™ 581/591 C11 was co-stained with Mito Tracker Red CMXRos to determine the mitochondrial levels of lipid ROS. Scale bars = 50 μm. Red indicates the reduced form of C11-BODIPY while green indicates the oxidised form of C11-BODIPY; the ratio of the oxidized form to the reduced form represents lipid peroxidation and the relative lipid peroxidation was the ratio of OE+Cis to NC+Cis. B Quantification of lipid ROS in HK-2 cells, n = 5. C Cell viability of HK-2 cells treated with the indicated reagents, n = 5. D The effect of mPGES-2 overexpression on the expression of ferroptosis markers under cisplatin. E Quantification of ferroptosis markers in mPGES-2 overexpressing or control cells under cisplatin, n = 3. F The effect of mPGES-2 overexpression on the expression of ferroptosis markers was reversed by hemin at 10 μM. G Quantification of ferroptosis markers in mPGES-2 overexpressing cells treated with hemin, n = 4, the samples were derived from the same experiment and gels/blots were processed in parallel. Data are expressed as mean ± SEM. Statistical significance was assessed using one-way ANOVA (C and G) or a two-tailed unpaired Student’s t-test (B and E). Exact P values are indicated.

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