Additional file 1: of Combination of Chymostatin and Aliskiren attenuates ER stress induced by lipid overload in kidney tubular cells

Figure A1. mRNA levels of RAS components in HK2 cells treated with palmitic acid. A. The mRNA levels of chymase, angiotensinogen, ACE in PA-treated HK2 cells with chymostatin and/or aliskiren. B. The mRNA levels of AT1R in PA-treated HK2 cells with chymostatin and/or aliskiren. Representative results of three independent experiments are shown. ATG: angiotensinogen; ACE: angiotensin converting enzyme; AT1R: angiotensin type 1 receptor; 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 treatment. * p < 0.05 compared with controls; # p < 0.05 compared with PA. (PPTX 52 kb

Additional file 2: of Combination of Chymostatin and Aliskiren attenuates ER stress induced by lipid overload in kidney tubular cells

Figure A2. Combination treatment with chymostatin and aliskiren couldn’t prevent ER stress in HK2 cells treated with tunicamycin (2 μg/ml). A. Tunicamycin induced upregulation of the ER markers (BiP and CHOP) expression in HK2 cells, neither pretreatment with chymostatin (5X10−5M) nor aliskiren (10− 8 M) attenuated ER stress induced by TM. B. Quantitative analysis of ER stress marker levels normalized to β-actin. Representative results of three independent experiments are shown. * p < 0.05 compared with controls. # p < 0.05 compared with TM. CTL, controls; TM, tunicamycin treatment group; TM + CMT, tunicamycin plus valsartan treatment; TM + Ali, tunicamycin plus aliskiren treatment; TM + CMT + Ali, tunicamycin plus chymostatin and aliskiren treatment. (PPTX 73 kb