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. 2018 Jul 31;17:183. doi: 10.1186/s12944-018-0818-1

Fig. 5.

Fig. 5

Combination treatment with chymostatin and aliskiren markedly prevented ER stress and apoptosis in HK2 cells treated with cholersterol (10 μg /ml) for 6 days. a Protein abundance of ER stress markers (BiP, IRE1α, PERK, CHOP and p-eIF2α/eIF2α) were upregulated after cholesterol treatment, which was prevented by cotreatment with chymostatin (5X10−5M) and aliskiren (10− 8 M). b Quantitative analysis of ER stress markers levels normalized to β-actin. c The ratio of p-eIF2α/eIF2α. d Protein abundance of Bax and caspase-3 was upregulated after cholersterol treatment, which was prevented by cotreatment with chymostatin and aliskiren, whereas the level of Bcl-2 was unchanged. e The ratio of Bax and Bcl-2. f Quantitative analysis of cleaved-caspased 3 levels normalized to β-actin. Representative results of three independent experiments are shown. * p < 0.05 compared with controls; # p < 0.05 compared with chol. CTL, controls; chol, cholesterol treatment group; chol+CMT, cholesterol plus chymostatin treatment; chol+Ali, cholesterol plus aliskiren treatment; chol+CMT + Ali, cholesterol plus chymostatin and aliskiren treatment