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Suppression of experimental crescentic glomerulonephritis by peroxisome proliferator-activated receptor (PPAR)gamma
Kazutaka Haraguchi1, Hiroki Shimura, Toshimasa Onaya
1Third Department of Internal Medicine, Yamanashi Medical University, 1110 Tamaho, Nakakoma, Yamanashi 409-3898, Japan. kazutaka@swallow.res.yamanashi-med.ac.jp
Background:
It has been recently reported that peroxisome proliferator-activated receptors (PPARs)gamma exist in various tissues and that they exibit anti-inflammatory effects.
Methods:
We investigated the effects of PPARgamma activators on the development of crescentic glomerulonephritis. Crescentic glomerulonephritis was induced by the injection of rabbit anti-rat glomerular basement membrane antibody in WKY rats.
Results:
Administration of troglitazone suppressed urinary protein excretion and crescent formation as indicated by crescent scores. Pioglitazone, a PPARgamma activator, mimicked the effect of troglitazone, but bezafibrate, a PPARalpha-activator, did not. Immunohistology revealed that troglitazone and pioglitazone inhibited the infiltration of ED-1-positive monocyte/macrophages and CD8-positive cells into glomeruli.
Conclusions:
In the present study, we demonstrated that PPARgamma activators exert antinephritic effects by suppressing the recruitment of inflammatory cells via a PPARgamma-dependent mechanism.
Insights
Peroxisome proliferator-activated receptors (PPARs)gamma activators reduced kidney inflammation and damage in a rat model of glomerulonephritis. These findings highlight PPARgamma’s role in mitigating kidney disease progression.
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Peroxisome proliferator-activated receptors (PPARs)gamma are found in various tissues.
- PPARgamma activation demonstrates anti-inflammatory properties.
Purpose of the Study:
- To investigate the therapeutic potential of PPARgamma activators in crescentic glomerulonephritis.
- To elucidate the mechanism by which PPARgamma activators impact kidney inflammation.
Main Methods:
- Crescentic glomerulonephritis was induced in WKY rats using rabbit anti-rat glomerular basement membrane antibody.
- Rats were treated with PPARgamma activators (troglitazone, pioglitazone) or a PPARalpha activator (bezafibrate).
- Urinary protein excretion, crescent formation, and inflammatory cell infiltration were assessed.
Main Results:
- PPARgamma activators significantly suppressed urinary protein excretion and crescent formation.
- Troglitazone and pioglitazone inhibited the infiltration of monocyte/macrophages and CD8+ cells into glomeruli.
- Bezafibrate, a PPARalpha activator, did not show similar protective effects.
Conclusions:
- PPARgamma activators possess significant antinephritic effects in experimental glomerulonephritis.
- The mechanism involves suppressing inflammatory cell recruitment in a PPARgamma-dependent manner.
- Targeting PPARgamma represents a potential therapeutic strategy for treating kidney diseases characterized by inflammation.
