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PPARγ Agonist Rosiglitazone Suppresses Renal mPGES-1/PGE2 Pathway in db/db Mice

Ying Sun1, Zhanjun Jia2, Gang Liu2

  • 1Department of Pharmacology, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Haidian District, Beijing 100191, China ; Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, UT, USA.

PPAR Research
|February 4, 2014
PubMed

Insights

Prostaglandin E2 (PGE2) is elevated in type-2 diabetic kidney disease. Activating peroxisome proliferator-activated receptor gamma (PPARγ) with rosiglitazone reduced PGE2 synthesis, suggesting mPGES-1 as a therapeutic target.

Area of Science:

  • Nephrology
  • Endocrinology
  • Biochemistry

Background:

  • Prostaglandin (PG) E2's role in type-1 diabetic nephropathy (DN) is known, but its involvement in type-2 DN is unclear.
  • Peroxisome proliferator-activated receptor (PPAR) γ interactions with PGE2 synthesis in type-2 DN require investigation.

Purpose of the Study:

  • To investigate the regulation of the PGE2 synthetic pathway in the kidneys of type-2 diabetic mice (db/db).
  • To examine the interaction between PPARγ and PGE2 synthesis in this model.

Main Methods:

  • Analysis of urinary PGE2, and kidney protein expressions of cyclooxygenase-2 (COX-2), microsomal PG E synthase-1 (mPGES-1), and other related enzymes in db/db mice.
  • Treatment with rosiglitazone (Rosi) to assess its effect on PGE2 pathway components and glomerular injury.
  • Immunohistochemistry to localize mPGES-1 expression in renal glomeruli.

Main Results:

  • db/db mice exhibited elevated urinary PGE2, COX-2, and mPGES-1 protein levels.
  • Rosiglitazone therapy significantly reduced urinary PGE2 and mPGES-1 expression, particularly in glomeruli.
  • A trend towards improved glomerular injury was observed following rosiglitazone treatment.

Conclusions:

  • PPARγ activation inhibits the renal mPGES-1/PGE2/EP4 pathway in type-2 diabetes.
  • Microsomal PG E synthase-1 (mPGES-1) emerges as a potential therapeutic target for type-2 diabetic nephropathy.

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