Skip to main content
. 2020 Jul 9;42(3):393–403. doi: 10.1038/s41401-020-0461-z

Fig. 6. Zonisamide alleviates HG-induced cardiac hypertrophy and apoptosis in cultured primary neonatal rat cardiomyocytes (NRCMs) via suppression of activated ER stress.

Fig. 6

NRCMs were pretreated with 5 mM 4-PBA (an inhibitor of ERS) or 10 ng/mL tunicamycin (Tm, an ERS inducer) for 2 h and then exposed to glucose (33 mM) in the presence or absence of ZNS (3 μM) for 24 h. a–b Representative and quantitative images showing the protein expression of ERS markers, including GRP78, XBP-1s, ATF6, p-PERK, PERK, ATF4, CHOP, and Hrd1. c Immunofluorescence staining of cardiomyocytes with phalloidin (red) and cell nuclei with DAPI (blue), Scale bar = 50 μm. d Quantitative analysis of cell surface area by ImageJ software. e–f Representative Western blotting and analysis of Bax and Bcl-2 expression. g–h Representative and quantitative images of GRP78, ATF6, p-PERK, PERK, ATF4, and CHOP expression. All values are the fold changes normalized to their control group. The results are presented as the means ± SEM (n = 6). *P < 0.05, **P < 0.01 vs. Con; #P < 0.05, ##P < 0.01 vs. HG; $P < 0.05, $$P < 0.01 vs. HG + ZNS.