Fig. 5
From: Targeting RNA-binding protein HuR to inhibit the progression of renal tubular fibrosis
Treatment with KH3 reduces renal mRNA expression and protein production of profibrotic, pro-inflammatory and proliferative markers in the ischemia–reperfusion (IR)-injured mouse kidney. a–e, Expression of TGFß1 (a), PAI-1 (b), NF-kBp65 (c), MCP-1 (d), and Nox2 (e) mRNA was determined by real-time RT/PCR. Changes in mRNA levels were determined by first correcting the amplification of GAPDH for each sample. f Representative Western blots of TGFß1, PAI-1, NF-kBp65, Nox2, p47phox, Nox4 and GAPDH and pERK1/2, t-ERK1/2 from contralateral (CTL) and ischemia–reperfusion (IR)-injured kidneys of untreated and KH3-treated mice. g–m The graphs summarize the results of band density measurements for TGFß1 (g), PAI-1 (h), NF-kBp65 (i), Nox2 (j), p47phox (k), Nox4 (l) and pERK1/2/t-ERK1/2 (m), respectively. *P < 0.05 vs. untreated contralateral kidney (CTL); #P < 0.05 vs. untreated IR-injured kidney (IR). n = 5/each group