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. 2022 Jan 3;12:790913. doi: 10.3389/fphar.2021.790913

FIGURE 2.

FIGURE 2

Evaluation of renal function following treatment with Eda-MNPs and controls. (A) Serum creatinine of mouse groups induced to have CI-AKI (Cis) and treated with Eda-MNPs or various controls. Bars represent the mean ± SEM. One-way ANOVA with Sidak’s posttest to compare to cisplatin control group. NS = p > 0.05; * = p < 0.05 (B) Blood urea nitrogen (BUN) of the same mouse groups as in panel (A). NS = p > 0.05; * = p < 0.05; *** = p < 0.001. (C) In non-fasted mice, serum creatinine of mouse groups with no AKI (N = 3), induced to have CI-AKI (Cis) (N = 4), or treated with Eda-MNPs (N = 5). Bars represent the mean ± SEM. One-way ANOVA with Sidak’s posttest to compare to cisplatin control group. Control vs Cis: 0.21 ± 0.029 vs 1.22 ± 0.303 mg/dl, p = * = 0.013; Cis vs Cis + Eda-MNP: 1.22 ± 0.303 vs 0.31 ± 0.018 mg/dl, p = * = 0.012 (D) In non-fasted mice, blood urea nitrogen (BUN) of the same mouse groups as in panel (C). One-way ANOVA with Sidak’s posttest to compare to cisplatin control group. Control vs Cis: 30.33 ± 1.86 vs 154 ± 16.27 mg/dl, p = *** = 0.000027; Cis vs Cis + Eda-MNP: 154 ± 16.27 vs 82.6 ± 5.91 mg/dl, p = ** = 0.0074. (E) IHC of NGAL expression in representative kidney sections from animals with each noted treatment, DAB detection (brown) and counterstained with haematoxylin (blue) (×10 magnification).