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. 2020 May;8(10):647. doi: 10.21037/atm-20-3768

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2020 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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BC attenuates AGE-induced cell apoptosis. (B) H9c2 cells were pre-treated with BC (40 µM) and then stimulated with AGEs (200 µg/mL) for 24 h. (A,B) Cell apoptosis was detected by Annexin V flow cytometry. (C) The protein expression levels of Bax, Bcl-2, and cleaved caspase-3 were detected by Western blot. (D,E) Semi-quantitative analysis of the relative levels of Bax, Bcl-2, and cleaved caspase-3. Each experiment was performed in triplicate. β-actin was used as loading control. *, P<0.05 vs. control group; ^#, P<0.05 vs. AGE-induced group. BC, beta-carotene; AGEs, advanced glycation end products; Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma-2.