ons 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.

Diabetic BTBR *ob/ob* mice developed renal lesions consisting of mesangial matrix accumulation accompanied by mesangiolysis, resulting in disrupted sites where capillary loops are anchored into the mesangium, which leads to the dilation of the capillary loop (Fig. [2b](#Fig2){ref-type="fig"}). In association with mesangial matrix accumulation, the glomeruli of BTBR *ob/ob* mice on vehicle exhibited a glomerular capillary rarefaction (*p* \< 0.001 versus WT mice), as revealed by immunofluorescence for CD31, a specific endothelial marker (Fig. [2c](#Fig2){ref-type="fig"}), and an increase in α-smooth muscle actin (α-SMA) expression (*p* \< 0.001 versus WT mice), a marker of mesangial cell activation (Fig. [2d](#Fig2){ref-type="fig"}). Tubular damage in BTBR *ob/ob* mice was mild, as reported previously^[@CR18]--[@CR20]^. Honokiol treatment significantly (*p* \< 0.001