Histological findings.

<p>Cardiac (A) or renal (B) mRNA levels of Col I and TGF-β in rats treated with Aldo-salt or with Aldo-salt plus TAK-242. *<i>p</i>< 0.05 vs control, #<i>p</i>< 0.05 vs Aldo-salt. (C)Representative images and quantitation of perivascular fibrosis in left ventricles of rats treated with Aldo-salt or with Aldo-salt plus TAK-242. *<i>p</i>< 0.05 vs control, #<i>p</i>< 0.05 vs Aldo-salt. (D) Histological staining with periodic acid Schiff (PAS), also showing tubulointerstitial damage of rats treated with Aldo-salt or with Aldo-salt plus TAK-242. *<i>p</i>< 0.05 vs control, #<i>p</i>< 0.05 vs Aldo-salt. n = 9, 200× magnification.</p

Cardiac and renal expression of TLR4 is increased in Aldo-salt-treated rats.

<p>(A and B) Rats were infused with Aldo-salt at 1 mg/kg/day for 4weeks, and cardiac mRNA levels (A) and protein levels (B) of TLR4 were assayed using qPCR and western blot, respectively. Rats were infused with Aldo-salt at 1 mg/kg/day for 4weeks, and renal mRNA levels (C) and protein levels (D) of TLR4 were assayed using qPCR and western blot, respectively. *<i>p</i>< 0.05.</p

Physiological and renal parameters in Aldo-salt–treated rats.

<p>Aldo = aldosterone; KW = kidney weight; BW = body weight.</p><p>Values are presented as mean ± SEM.</p><p>*<i>p</i><0.05 vs. control</p><p>^#<i>p</i><0.05 vs. Aldo-salt group.</p><p>Physiological and renal parameters in Aldo-salt–treated rats.</p

TAK-242 suppresses renal inflammation and fibrosis caused by Aldo-salt <i>in vivo</i>.

<p>(A-C) Renal mRNA levels of TNF-α, MCP-1 and IL-1β in rats treated with Aldo-salt or with Aldo-salt plus TAK-242. *<i>p</i>< 0.05 vs control, #<i>p</i>< 0.05 vs Aldo-salt. (D) Renal protein levels of TNF-α, MCP-1 and IL-1β in rats treated with Aldo-salt or with Aldo-salt plus TAK-242 were assayed using ELISA. *<i>p</i>< 0.05 vs control, #<i>p</i>< 0.05 vs Aldo-salt.</p

TAK-242 suppresses Aldo-salt-induced EMT.

<p>Renal mRNA (A) and protein (B) expression of E-cadherin (an epithelial marker), and Fibronectin and a-SMA (mesenchymal markers) were assayed in rats treated with Aldo-salt or with Aldo-salt plus TAK-242. TAK-242 reversed the Aldo-salt–induced renal epithelial-mesenchymal transition. *<i>p</i>< 0.05 vs control, #<i>p</i>< 0.05 vs Aldo-salt.</p

HS increases and CCL20 antibody decreases Th17-related cytokines in IgAN mice.

<p>(A): Renal CCL20 concentrations of each groups; (B): Renal IL-17A concentrations of each groups; (C): Renal IL-21 concentrations of each groups; (D): Renal IL-6 concentrations of each groups. ^#<i>vs</i> control group, <i>P</i><0.05; ^*<i>vs</i> IgAN group, ^&<i>vs</i> HS-IgAN group <i>P</i><0.05.</p

HS increases and CCL20 antibody decreases ACR in IgAN mice.

<p>^#<i>vs</i> control group, <i>P</i><0.05; ^*<i>vs</i> IgAN group, <i>P</i><0.05; ^&<i>vs</i> HS-IgAN group, <i>P</i><0.05.</p

HS worsens and CCL20 antibody improves renal damage in IgAN mice.

<p>Representative images of HE-stained (A, 400×), PAS-stained (B, 400×), Immunofluorescence (C, 200×) and transmission electron micrographs (D) kidney sections from mice as indicated. For immunofluorescence staining, IgA antibody was used. The arrows in D point to high electron dense deposition in glomerular mesangial region.</p

HS worsen and CCL20 antibody improves lung damage in IgAN mice.

<p>Representative images of HE stained lungs from mice as indicated (200×).</p

HS increases and CCL20 antibody decreases abnormal glomeruli in IgAN mice.

<p>PAS-stained kidney sections were evaluated for the presence of abnormal glomeruli. ^#<i>vs</i> control group, <i>P</i><0.05; * <i>vs</i> IgAN group, <i>P</i><0.05; ^&<i>vs</i> HS-IgAN group, <i>P</i><0.05.</p