Research Article

Bailcalin Protects against Diabetic Cardiomyopathy through Keap1/Nrf2/AMPK-Mediated Antioxidative and Lipid-Lowering Effects

Figure 7

BAI exerted antioxidant effects via AMPK-dependent effects on Nrf2. (a) BAI increased Nrf2 but not p-AMPKα in a concentration-dependent manner. (b) BAI restored the expression and nucleus translocation of Nrf2 in HG/Pal-treated NRCM. (c) BAI restored p-AMPKα in HG/Pal-treated NRCM. (d) BAI inhibited the expression of 4-HNE, BAX, and cleaved caspase 3 (c-caspase 3) induced by HG/Pal treatment in NRCM. (e) Representative Western blots of Nrf2 and HO-1 expressions with or without Nrf2 silencing; (f) representative blots of p-AMPKα and total AMPKα (T-AMPKα) expressions with or without AMPKα silencing; mRNA expressions of (g) ANP, (h) BNP, and (i) NQO1; examination accumulation of (j) MDA and (k) GSSG; mRNA expressions of (l) CPT-1, (m) PGC1-α, and (n) BAX. HG: high glucose; Pal: palmitate; BAI: Bailcalin. β-Actin was selected as the internal reference. The final concentration of 20 μM BAI was used in experiments; each experiment was repeated three times independently. compared with the indicated group.
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