Agonist of peroxisome proliferator-activated receptor-γ, rosiglitazone, reduces renal injury and dysfunction in a murine sepsis model

Lee, Sik; Kim, Won; Kang, Kyung Pyo; Moon, Sang-Ok; Sung, Mi Jeong; Kim, Duk Hoon; Kim, Hyung Jin; Park, Sung Kwang

doi:10.1093/ndt/gfh705

Cited by 51 publications

(36 citation statements)

References 18 publications

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“…Previous in vivo studies demonstrated that PPAR-g agonists reduced interstitial macrophage infiltration in progressive renal disease in the rat and a model of murine sepsis. 17,18,36 On the other hand, Panzer reported that MCP-1 expression and monocyte-macrophage infiltration were enhanced during the induction phase in a model of experimental glomerulonephritis. 37 These different findings may be attributable to the different times studied after induction of glomerulonephritis.…”

Section: Discussionmentioning

confidence: 99%

PPAR-γ agonist attenuates renal interstitial fibrosis and inflammation through reduction of TGF-β

Kawai

Takao

Doi

et al. 2009

Laboratory Investigation

189

125

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Thiazolidinediones (TZDs), synthetic peroxisome proliferator-activated receptor (PPAR)-g ligands, have a central role in insulin sensitization and adipogenesis. It has been reported that TZDs exert protective effects in both diabetic and nondiabetic models of renal disease, although the exact mechanism is not well understood. In particular, only a few studies have reported the renoprotective effects of TZDs in nondiabetic models of tubulointerstitial fibrosis and inflammation. Therefore, we investigated the anti-fibrotic and anti-inflammatory effects of the TZD troglitazone in the mouse model of unilateral ureteral obstruction (UUO). C57BL/6J mice underwent UUO and were studied after 3 and 7 days. Animals were divided into three groups and received control vehicle, troglitazone (150 mg/kg per day) or troglitazone (300 mg/kg per day) by gavage. Kidneys were harvested for morphological, mRNA and protein analysis. Reversetranscriptase-PCR was used to assess the expression of transforming growth factor-b1 (TGF-b1) and the TGF-b1 type I receptor (TGFbR-I). Protein expression was assessed by western blotting (TGFbR-I) and immunostaining (TGFbR-I, a-smooth muscle actin (a-SMA), type I collagen (collagen I), F4/80, and proliferating cell nuclear antigen (PCNA)). The expression of a-SMA, collagen I, and F4/80 was decreased in mice treated with troglitazone compared with the control group. The numbers of PCNA-positive interstitial cells were decreased in mice treated with troglitazone. TGF-b1 mRNA and TGFbR-I mRNA and protein expression were decreased in the group treated with troglitazone compared with the control group. The beneficial effects of troglitazone treatment were also dose dependent. PPAR-g agonist significantly reduced TGF-b and attenuated renal interstitial fibrosis and inflammation in the model of UUO.

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Section: Discussionmentioning

confidence: 99%

PPAR-γ agonist attenuates renal interstitial fibrosis and inflammation through reduction of TGF-β

Kawai

Takao

Doi

et al. 2009

Laboratory Investigation

189

125

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“…Furthermore, it reduced TGF-beta1-induced fibronectin expression in mouse glomerular mesangial cells by inhibiting activator protein-1 (AP-1) (56,58,60). In a murine sepsis model, a reduction in renal injury and dysfunction has also been reported in association with the anti-inflammatory effects of glitazones (61).…”

Section: Possible Nephroprotective Actions Of Pparg Agonistsmentioning

confidence: 97%

Peroxisome proliferator-activated receptor gamma agonists in renal disease

Iglesias

Díez

2006

eur j endocrinol

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Type 2 diabetes is a well recognised cause of chronic renal failure (CRF). Only few oral antidiabetic drugs can be used for treating type 2 diabetes in patients with CRF. Among them are repaglinide, a rapid-acting prandial insulin releaser, and peroxisome proliferator-activated receptor gamma (PPARg) agonists, such as rosiglitazone and pioglitazone. These compounds are metabolised in the liver, therefore accumulation of the drug and the risk of severe and prolonged hypoglycaemia are minimised. PPARg receptors are expressed in many tissues including the kidney. Recently, numerous healthful effects of PPARg agonists on several aspects related to renal function have been increasingly reported. These drugs have shown to possess many advantageous anti-inflammatory, haemodynamic, vascular and metabolic effects. In the present paper we have reviewed the more recent experimental studies that evaluated these potential beneficial effects of PPARg agonists on renal function and revised the results of their utilisation in patients with different degrees of renal impairment, in dialysis patients, and in patients with diabetes mellitus after kidney transplantation. Finally, tolerability and safety profile of PPARg agonists in patients with reduced glomerular filtration rate are also analysed. European Journal of Endocrinology 154 613-621

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“…Increased innate immune activation, neutrophil and macrophage infiltration, and enhanced TNF-␣ production are observed in infections (83), cisplatin nephropathy (73,114), diabetic nephropaty (38), antiglomerular basement membrane nephropathy (142), obstructive nephropathy (134), etc. In such situations stimuli for TNF-␣ production include activation of Toll-like receptor 4 in response to LPS (85), oxidative stress (30), antibody deposition, and complement activation (142,159).…”

Section: Tumor Necrosis Factor-␣ In the Kidney: Synthesis And Secretionmentioning

confidence: 99%

Tumor necrosis factor-α: regulation of renal function and blood pressure

Ramseyer

Garvin

2013

American Journal of Physiology-Renal Physiology

149

106

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Agonist of peroxisome proliferator-activated receptor-γ, rosiglitazone, reduces renal injury and dysfunction in a murine sepsis model

Cited by 51 publications

References 18 publications

PPAR-γ agonist attenuates renal interstitial fibrosis and inflammation through reduction of TGF-β

PPAR-γ agonist attenuates renal interstitial fibrosis and inflammation through reduction of TGF-β

Peroxisome proliferator-activated receptor gamma agonists in renal disease

Tumor necrosis factor-α: regulation of renal function and blood pressure

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