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. 2019 May 14;10:559. doi: 10.3389/fphys.2019.00559

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Copyright © 2019 Qian, Du, Jiang, Lin and Yao.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Assessment of kidney function and renal histological injury in WT and SMN+/– mice subjected to IRI. The I/R-induced AKI mouse model was induced in WT and SMN+/– mice. Blood and kidney tissues were collected at 24 h after I/R, as described in the Materials and Methods. (A) Western blot analysis of SMN protein expression in I/R-induced AKI in WT and SMN+/– mice. GAPDH was used as the loading control. (B) Serum creatinine (Scr, n = 10) and blood urea nitrogen (BUN, n = 8). (C) Representative images of hematoxylin and eosin (HE) staining. Original magnification, 400×. Bar = 50 μm. (D) Semiquantitative assessment of tubular damage. WT sham, SMN+/– sham, and SMN+/– IRI, n = 8; WT IRI, n = 11. (E) Real-time PCR analysis of kidney KIM-1 mRNA expression. Data are expressed as the mean ± SD; (^∗p < 0.0001 vs. sham-operated WT mice; ^∗∗p < 0.05 vs. ischemic WT mice under the same experimental conditions).