Figure 1
From: Urinary miR-21 as a potential biomarker of hypertensive kidney injury and fibrosis
Deoxycorticosterone acetate (DOCA)-salt treatment induced tubulointerstitial lesions. (A) Representative images of hematoxylin-eosin-stained kidney sections of mice under control conditions and DOCA-salt-treated conditions for 2 days (DOCA-2), 4 days (DOCA-4), and 8 days (DOCA-8). DOCA-treated mice showed gradually aggravated tubular dilatation/atrophy (*), epithelial cell necrosis, and interstitial edema. The area of tubulointerstitial injury, as well as the entire cortical area, in 10 high-power fields was measured with ImageJ software. (B) The degree of tubulointerstitial injury was evaluated as a ratio relative to the entire cortical area. (C) The ratio of kidney weight (KW)/body weight (BW) was increased after DOCA-salt treatment. (D,E) Urinary albumin (Alb) and N-acetyl-beta-D- glucosaminidase (NAG) levels were elevated by the treatment with DOCA-salt. Serum creatinine (Cre, F) levels in the mice treated with DOCA-salt for 8 days were comparable to the control mice. *P < 0.05, **P < 0.01 compared to the basal condition; # P < 0.01; n = 8, error bars, mean ± SD.
