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. 2020 Feb 6;32:101453. doi: 10.1016/j.redox.2020.101453

Fig. 4.

Fig. 4

Blockade of Nrf2 activation by ML385 suppresses Tsg101-mediated cardio-protective effects. (A) Schematic diagram depicting the experimental protocol for intraperitoneal (i.p.) injection of ML385 daily for 3 times, 24 h after the last injection, heart samples were collected for a series of experiments. (B) Representative Western-blots and (C) quantitative analysis validating the inhibitory effects of ML385 on the nuclear levels of Nrf2 in WT- and TG-hearts, and (D) RT-PCR analysis for Nrf2-target gene expression in mouse hearts with or without ML385-injection; *, p < 0.05 vs. WT-controls, n = 4. Cardiac functional recovery assessed by (E) LV dp/dt (max) and (F) LV dp/dt (min) in ML385-treated WT- and TG-hearts during ex vivo I/R (45min/1 h). n = 5 for each group. *, p < 0.05 vs. WT-controls. (G) Total LDH levels in coronary effluent collected during the first 10 min of reperfusion. *, p < 0.05 vs. WT-controls. (H) Caspase-3 activity in the WT- and TG-hearts, pretreated with or without ML385, upon ex vivo I/R (45min/1 h). *, p < 0.05 vs. WT-controls. (I) Representative images and (J) quantification analysis of Dihydroethidium (DHE) staining in heart sections from WT- and TG-hearts, pretreated with or without ML385, upon ex vivo I/R (45min/5min). *, p < 0.05. (K) Representative infarction images of mouse hearts upon in vivo I/R (1h/24 h) and (L) quantitative results of infarction size and (M) the ratio of risk region to left ventricular (LV) area. *, p < 0.05 vs. WT-controls. n.s. stands for no significance.