Figure 3
Effects of intravenous injection of HLSC-derived CM into AKI mice. Creatinine (A) and BUN (B) were measured in mice treated with vehicle alone and in HLSC-derived CM-treated mice five days after glycerol injection and in healthy control (ctrl) mice. Data are expressed as mean ± SD; ANOVA with Dunnet’s multicomparison test: *P <0.05 HLSC-derived CM-treated AKI mice versus vehicle-treated AKI mice. (C) Comparison of HLSC-derived CM injections on tubular morphology at day 5 after AKI induction. Data are expressed as mean ± SD of hyaline cast and necrotic tubules observed under high power (original magnification: ×400). ANOVA with Dunnet’s multicomparison test: *P <0.05 HLSC-derived CM-treated AKI mice versus vehicle-treated AKI mice. (D) Representative micrographs of renal histology of healthy SCID mice and of AKI mice treated with vehicle alone or injected intravenously with concentrated CM derived from different quantities of HLSCs (CM (3.5 × 105), CM (10 × 105), CM (20 × 105)) (original magnification: ×200). AKI, acute kidney injury; ANOVA, analysis of variance; BUN, blood urea nitrogen; CM, conditioned medium; HLSCs, human liver stem cells; SCID, severe–combined immune-deficient; SD, standard deviation.