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. 2015 Dec 23;10(12):e0145666. doi: 10.1371/journal.pone.0145666

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© 2015 Ma et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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Fig 3 — Histological staining with PAS and hematoxylin shows the structure of kidney tubules in (A) a normal mouse. In comparison, there is severe damage to tubules (dilation, atrophy, cell loss) at day 15 of glomerulonephritis in (B) a mouse receiving no treatment and (C) a mouse receiving vehicle, which is attenuated in (D) a mouse treated with BR-4628. Graphs show (E) the number of activated caspase-3+ apoptotic cells in tubules in the kidney cortex and (F) the gene expression of kidney injury molecule-1 (KIM-1) in kidneys from normal control (NC) mice and mice with glomerulonephritis (GN) receiving no treatment (No Tx), vehicle or BR-4628. Magnification: (A-D) x400. Graph Data = mean ± SEM; n = 8. *p<0.05, ***p<0.001, NS = not significant.