Fig. 4
From: Targeting RNA-binding protein HuR to inhibit the progression of renal tubular fibrosis
Treatment with KH3 reduces tubular a-SMA staining and renal protein levels of fibrotic markers following ischemia–reperfusion (IR) injury. a OCT kidney sections from mice following IR injury without and with KH3 treatment were stained with a-SMA (green) and DAPI/DNA (blue) and analyzed using confocal microscopy. Magnification, ×200. b The graphs summarized the results of a-SMA deposition quantified by image-J. c Western blots of a-SMA, FN, N-cadherin, vimentin and GAPDH from CTL and IR-injured kidneys of KH3-untreated and treated mice. Molecular weight was labelled on the right. N = 5 animals/group. d–g The graphs summarize the results of band density measurements for a-SMA (d), FN (e), N-cadherin (f) and Vimentin (g). h–j mRNA expression of Col-I (h), Col-III (i) and FN (j) in the kidney following IR injury. *P < 0.05 vs. untreated contralateral kidney (CTL); #P < 0.05 vs. untreated IR-injured kidney (IR)