Fig 1: In vivo assessment of hidrosmin effect in experimental DN: (a) evolution of UACR levels in diabetic groups (control, D; hidrosmin-treated, D + H) along the study; (b) KIM-1 protein concentration in urine samples at final point; (c) real-time PCR analysis of Kim-1 and Ngal in renal cortex. Values normalized by 18S are expressed in arbitrary units (a.u.); (d) representative images of PAS staining (magnification ×400) and assessment of glomerular (G), tubulointerstitial (TI), and total kidney semiquantitative score. Scatter dot plots represent individual values and the mean ± SEM of n = 6–9 animals (D group) and n = 7–11 animals (D + H group). * p < 0.05, ** p < 0.01, and *** p < 0.001 vs. D.
Fig 2: DKD progression rates vary among HFD-fed mice. (A) Urinary albumin/creatinine ratio (UACR) and urinary KIM-1/creatinine ratio (UKCR); (B) Renal protein expression of KIM-1 and antioxidant enzyme SOD2 (C) Histological staining: Hematoxylin and Eosin (H&E) and Pico-Sirius Red (PSR). * p < 0.05, ** p < 0.01, *** p < 0.001. HFD-2: mice with advanced kidney injury, HFD-1: mice with mild–moderate kidney injury.
Fig 3: The development and progression of DKD in high-fat diet (HFD) fed animals at week 9 and week 32. (A) Urinary albumin/creatinine ratio (UACR), Kidney injury marker (KIM)-1 to creatinine ratio, and plasma creatinine. (B) Renal mRNA expression of oxidative stress and inflammation markers. * p < 0.05, *** p < 0.001 vs. Ctrl.
Fig 4: Effect of Betulinic acid pretreatment on (A) serum KIM-1 level, (B) serum NGAL level, and (C) serum creatinine. Cisplatin (25 mg/kg, i.p) was used for nephrotoxicity induction. Betulinic acid (30 mg/kg and 50 mg/kg orally) was given for 10 days. Data expressed as mean ± SD (n = 6/group), a means significant vs. control, b means significant vs. cisplatin group. p ? 0.05.
Fig 5: Treatment with quercetin inhibits SARS-CoV-2 N protein-induced AKI in 8-week-old db/db mice. (A) PAS staining. (B) Semi-quantitative assessment of tubular necrosis. (C) Serum creatinine. (D) Serum level of blood urea nitrogen (BUN). (E) Immunohistochemistry for expression of KIM-1 in the kidney. (F) Semi-quantitative analysis of renal KIM-1 protein expression. (G) Levels of urinary KIM-1. Results show that quercetin at 150 mg/kg can inhibit kidney-specific SARS-CoV-2 N-induced (300 μg/per mice) AKI in 8-week-old db/db mice by significantly blocking tubular necrosis (asterisk), lowering serum levels of creatinine and BUN, and suppressing the expression of renal and urinary KIM-1. Each dot represents one mouse, and data are expressed as mean ± SEM. ∗∗∗∗p < 0.0001 versus empty vector control group (db/db-EV); ####p < 0.0001 versus DMSO-treated control group ( db/db-NP+DMSO). g, glomerulus. Scale bar, 100 μm.
Supplier Page from Abcam for Mouse KIM1 ELISA Kit (TIM-1)