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. 2017 Jan 31;18(2):305. doi: 10.3390/ijms18020305

Figure 3.

Figure 3

Induction of HO-1 (hemeoxygenase-1) and thioredoxin by losartan (A) and reversal of inhibitory effect of losartan on the tunicamycin-induced ER stress by HO-1 inhibitor (PPIX) and thioredoxin inhibitor (PX12) (B). Proximal tubular cells were incubated with tunicamycin (TM, 0.2 µM) with or without losartan (losar, 10 µM) for 24 h. Expression of heme oxygenase-1 (HO-1) and thioredoxin was examined by Western blot analysis (A). Proximal tubular cells were incubated with tunicamycin (TM, 0.2 µM) with or without losartan (losar, 10 µM), heme oxygenase-1 inhibitor (PPIX, 20 µM), and thioredoxin inhibitor (PX12, 25 µM) for 24 h. Expression of GRP78 and p-eIF2α was examined by Western blot analysis (B). The relative densities of the bands for HO-1, thioredoxin, GRP78, and p-eIF2α were normalized to those for actin for standardization. Representative blots and quantitative analysis from three independent experiments were shown. Results were expressed as n-fold increase over control as mean ± S.E. #: p < 0.05 vs. con (control); ##: p < 0.05 vs. TM; ###: p < 0.05 vs. TM + losar.