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Fig. 2 | Journal of Inflammation

Fig. 2

From: High-fat diet-induced obesity causes an inflammatory microenvironment in the kidneys of aging Long-Evans rats

Fig. 2

Renal inflammation and fibrosis in 18-month-old LEV rats. (a) PAS-stained renal tissues of 75-week-old rats show only subtle changes in those rats receiving a control diet (CD, upper two panels) compared to those fed a high-fat diet (HFD, lower two panels). In contrast to the CD, the HFD led to widespread tubular dilatation (open triangles), massive infiltration of mononuclear cells (filled triangles), and enhanced glomerulosclerosis (arrows) and tubular protein casts (stars). (b) The renal infiltration of ED1-positive monocytes/macrophages (Mo/MΦ) was significantly enhanced in rats fed a HFD. (c) Immunohistochemical staining of a-smooth muscle actin (aSMA) shows, next to the constitutive staining of smooth muscle cells, enhanced staining of profibrotic myofibroblasts in the tubulointerstitium of rats fed a HFD. (d)-(k) Quantification of the renal changes shows significantly enhanced tubulointerstitial fibrosis (d), glomerulosclerosis (e) and tubular damage (f) in the HFD-fed rats compared to CD-fed rats with a tendency for increased expression of aSMA (g) and type III collagen (h). The number of foci with renal immune infiltrates (i) and the number of infiltrating Mo/MΦ (j) increased significantly by HFD compared to the CD. K. HFD-fed rats showed a significantly enlarged area of tubular protein casts, pointing to enhanced proteinuria. Statistical significance (HFD vs. CD) was determined using two-way t-tests or Mann-Whitney-U test and is denoted by * for p ≤ 0.05, ** for p ≤ 0.01 or *** for p ≤ 0.001

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