Baicalin improves isoproterenol-induced cardiac remodeling by regulating the Nrf2-dependent signaling pathway

Fig. 1. Baicalin ameliorates cardiac dysfunction induced by isoproterenol in mice. (A) The chemical structure of baicalin (upper) and the survival rate of mice in each group (down) (log-rank: P < 0.01, n = 11 per group). (B) Cardiac morphology and statistical results of HW/BW and LW/BW. (C) Representative M-mode echocardiograms of long axis views and the quantitative analysis of LVEF, LVFS, LVIDd and LVPWd. (D) Pathological changes observed through H&E staining. Data are expressed as mean ± SD. *P<0.05 vs. Con group; #P<0.05 vs. ISO group (n = 3 for each group)

Fig. 2. Baicalin alleviates myocardial hypertrophy and ferroptosis induced by isoproterenol in mice. (A-B) Effects of Bai on the protein expression of ANP, BNP, β-MHC evaluated by western blot analysis. (C-D) Effects of Bai on the protein expression of TGF-β, Collagen I and Fib evaluated by western blot analysis. (E-F) Effects of Bai on the protein expression of GPX4, PTGS2 and FTH1 evaluated by Western blot analysis. Data are expressed as mean ± SD. *P<0.05 vs. Con group; #P<0.05 vs. ISO group (n = 3 for each group)

Fig. 3. Baicalin mitigates myocardial hypertrophy by Nrf2 signaling pathways in mice. (A-B) Effects of Bai on the protein expression of IL-6, TNF-α, CAT and SOD1 evaluated by western blot analysis. (C-D) Effects of Bai on the protein expression of p-Nrf2, Nrf2, HO-1, and NQO1 evaluated by western blot analysis. Data are expressed as mean ± SD. *P<0.05 vs. Con group; #P<0.05 vs. ISO group (n = 3 for each group)

Fig. 4. Baicalin effects cardiac dysfunction after inhibition of Nrf2 by ML385 in mice. (A) Cardiac morphology of each group. (B) Pathological changes and fibrosis of each group observed through masson staining. (C) Statistical results of HW/BW and LW/BW. Data are expressed as mean ± SD. *P<0.05 vs. Con group; #P<0.05 vs. ISO group; &P<0.05 vs. ISO + Bai group (n = 3 for each group)

Fig. 5. Baicalin alleviates myocardial hypertrophy and ferroptosis after inhibition of Nrf2 by ML385 in mice. (A-B) Effects of Bai on the protein expression of ANP, BNP, β-MHC evaluated by western blot analysis. (C-D) Effects of Bai on the protein expression of TGF-β, Collagen I and Fib evaluated by western blot analysis. (E-F) Effects of Bai on the protein expression of GPX4, PTGS2 and FTH1 evaluated by western blot analysis. Data are expressed as mean ± SD. *P<0.05 vs. Con group; #P<0.05 vs. ISO group; &P<0.05 vs. ISO + Bai group (n = 3 for each group)

Fig. 6. Effects of baicalin on Nrf2 signaling pathway after inhibition of Nrf2 by ML385 in mice. (A-B) Effects of Bai on the protein expression of IL-6, TNF-α, CAT and SOD1 evaluated by western blot analysis. (C-D) Effects of Bai on the protein expression of p-Nrf2, Nrf2, HO-1, and NQO1 evaluated by western blot analysis. Data are expressed as mean ± SD. *P<0.05 vs. Con group; #P<0.05 vs. ISO group; &P<0.05 vs. ISO + Bai group (n = 3 for each group)

Fig. 7. Bai attenuates ISO-induced cardiac hypertrophy in vitro through Nrf2-related ferroptosis. (A) The cell surface area of HL-1 cells was assessed by FITC-conjugated phalloidin staining (green for F-actin, blue for DAPI). (B) Effects of Bai on the protein expression of GPX4, PTGS2 and FTH1 evaluated by western blot analysis in HL-1 cells. (C) Effects of Bai on the expression of GSH, MDA, ROS and Fe2+ in HL-1 cells. Data are expressed as mean ± SD. *P < 0.05 vs. Con group; #P<0.05 vs. ISO group, &P<0.05 vs. ISO + Bai group (n = 3 for each group)