Fig. 1From: Combination of Chymostatin and Aliskiren attenuates ER stress induced by lipid overload in kidney tubular cellsCombination treatment with chymostatin and aliskiren markedly prevented ER stress in HK2 cells treated with palmitic acid (0.6 mM) for 24 h. a Protein abundance of ER stress markers (BiP, IRE1α, PERK, ATF4, pS51-eIF2α, eIF2α, and CHOP) were upregulated after PA treatment, which was prevented by cotreatment with chymostatin (5X10−5M) and aliskiren (10− 8 M). b Quantitative analysis of ER stress marker levels normalized to β-actin. c Ratio of pS51-eIF2α and eIF2α. d Protein abundance of CHOP normalized to β-actin. Representative results of three independent experiments are shown. * p < 0.05 compared with controls; # p < 0.05 compared with PA. BiP, ER chaperone immunoglobulin heavy chain binding protein; IRE1α, inositol requiring protein 1α; PERK, protein kinase RNA (PKR)-like ER kinase; eIF2α: eukaryotic initiation factor 2α; ATF4, activating transcription factor 4; CHOP, C/EBP homologous protein. CTL, controls; PA, palmitic acid treatment group; PA + CMT, palmitic acid plus chymostatin treatment; PA + Ali, palmitic acid plus aliskiren treatment; PA + CMT + Ali, palmitic acid plus chymostatin and aliskiren treatmentBack to article page