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. 2020 May 8;12(5):434. doi: 10.3390/pharmaceutics12050434

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Folic acid (FA) induces AKI and renal fibrosis development. (A) Measurement of body weights of C57BL/6 mice. Mice were i.p. injected with 250 mg/kg FA one time at day 0. * p < 0.05 compared with normal. Renal function was assessed at 2, 7, 14, 28 and 35 days postinjection by measuring blood urea nitrogen (BUN) (B) and creatinine (C) levels. * p < 0.05 compared with normal. (D) Representative kidney sections in mice were stained with H+E and examined by microscopy. Scale bar = 50 μm.

Folic acid (FA) induces AKI and renal fibrosis development. (A) Measurement of body weights of C57BL/6 mice. Mice were i.p. injected with 250 mg/kg FA one time at day 0. * p < 0.05 compared with normal. Renal function was assessed at 2, 7, 14, 28 and 35 days postinjection by measuring blood urea nitrogen (BUN) (B) and creatinine (C) levels. * p < 0.05 compared with normal. (D) Representative kidney sections in mice were stained with H+E and examined by microscopy. Scale bar = 50 μm.