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

Figure 7.

Figure 7

PI3K/Akt/mTOR is essential in BC protection of AGE-induced cardiac injuries. H9c2 cells were pre-treated with BC (40 µM) and LY294002 (LY, 10 µM) and then stimulated with AGEs (200 µg/mL) for 24 h. (A) The expression levels of Bax and Bcl-2 were detected by Western blot. (B) Semi-quantitative analysis of the relative levels of Bax and Bcl-2. (C) Cell apoptosis rate. (D) Intracellular ROS production. (E) SOD activity. (F) The expression levels of ATF4, GRP78, and CHOP were detected by Western blot. (G) Semi-quantitative analysis of the relative levels ofATF4, GRP78, and CHOP. (H) The expression levels of beclin 1, p62, and LC3 were detected by Western blot. (I) Semi-quantitative analysis of the relative level of beclin 1, p62 and LC3. (J) The quantification of the number of LC3 puncta. Each experiment was performed in triplicate. *, P<0.05 vs. control; #, P<0.05 vs. AGEs; $, P<0.05 vs. AGEs + BC. PI3K/Akt/mTOR, Phosphatidyl inositol 3-kinase/Akt/mammalian target of rapamycin; BC, beta-carotene; AGEs, advanced glycation end products; Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma-2; ROS, reactive oxygen species; SOD, superoxide dismutase; ATF4, activating transcription factor 4; GRP78, glucose-regulated protein 78; CHOP, CCAAT/enhancer-binding protein homologous protein; LC3, microtubule-associated protein 1 light chain 3.