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. 2020 May 21;10:8418. doi: 10.1038/s41598-020-65423-0

Figure 2.

Figure 2

SIRT3 activation through honokiol treatment limits albuminuria, glomerular structural lesions and inflammation in diabetic mice. (a) Urinary albumin excretion at 14 weeks of age in BTBR WT mice (n = 9) and BTBR ob/ob mice treated with vehicle (n = 6) or honokiol (n = 9). (b) Periodic acid-Schiff-stained sections of representative glomeruli and quantification from BTBR WT mice (n = 9) and from diabetic mice treated with vehicle (n = 6) or honokiol (n = 9) at 14 weeks of age showing glomerular lesions, consisting of mesangial matrix expansion (arrowheads) and mesangiolysis (asterisk). Scale bars: 20 μm. (c,d) Representative images and quantification of glomerular CD31 (c) and α-SMA expressions (d) in BTBR WT mice (n = 9) and in BTBR ob/ob mice treated with vehicle (n = 6) or honokiol (n = 9) at 14 weeks of age. Nuclei were stained with DAPI and renal structure with lectin FITC-wheat germ agglutinin (WGA). Scale bars: 20 μm. (e) Representative images and quantification of glomerular accumulation of Mac-2-positive monocytes/macrophages in BTBR WT mice (n = 9) and in BTBR ob/ob mice treated with vehicle (n = 6) or honokiol (n = 9) at 14 weeks of age. Scale bars: 20 μm. Data are mean ± SEM and were analyzed by one-way ANOVA followed by Tukey’s multiple comparisons test, ***p < 0.001 vs BTBR WT mice; #p < 0.05, ###p < 0.001 vs BTBR ob/ob + vehicle.