Fig. 7

Inhibition of miR-92a-1-5p protected renal function in db/db diabetic mice and ameliorated diabetic nephropathy (DN) progression in vivo. A Urinary exosomal miR-92a-1-5p levels, albumin-creatinine ratio (ACR), neutrophil gelatinase-associated lipocalin/creatinine (NGAL/Cr) and kidney injury molecule 1/creatinine (KIM-1/Cr) expressions were measured in db/db mice (n = 5) and db/m mice (n = 5) at 12th week. B The correlation between urinary exosomal miR-92a-1-5p levels and urinary ACR, NGAL/Cr and KIM-1/Cr in mice at 12th week. C Flow chart of intervention study in vivo. D Urinary ACR and NGAL/Cr levels were measured in db/db mice treated with antagomir-92a-1-5p (n = 4) compared with those treated with negative control (NC) antagomir (n = 4). E Serum urea nitrogen (UN) and creatinine were examined in db/db mice treated with antagomir-92a-1-5p compared to those treated with NC antagomir. Exosomal miR-92a-1-5p in the urine of mice was isolated, and then assessed by qRT-PCR. Urine albumin was measured using immunoturbidimetric assay. Serum UN and urine creatinine levels were determined using the enzymatic method. Serum creatinine was measured using the compensated Jaffé (kinetic alkaline picrate) method. The concentration of NGAL and KIM-1 in urine was measured using enzyme-linked immunosorbent assay (ELISA). F Periodic acid-schiff stain of kidneys in mice. G-I The expressions of RCN3, ATF-6, and N-cadherin in MCs of kidneys in mice (NC antagomir (n = 4), antagomir-92a-1-5p (n = 4)). The kidney sections were co-stained with RCN3, ATF-6, and N-cadherin (brown) and α-SMA (green), as the marker of MCs. The images quantification was performed using the IHC Profiler Plugin of ImageJ Software. The bar graph represents the mean ± S.E.M. *p < 0.05, **p < 0.01, ***p < 0.001 by Student’s t-test. p-value of correlation was analyzed by Spearman analysis