Cox-2 inhibition attenuates cardiovascular and inflammatory aspects in monosodium glutamate-induced obese rats

N V Cunha1, S B de Abreu, C Panis

  • 1Department of Physiological Sciences, State University of Londrina, Londrina, Paraná, Brazil.

Life Sciences
|August 7, 2010
PubMed
Abstract

Insights

Monosodium glutamate (MSG) induced obesity in rats leads to hypertension and inflammation. Cyclooxygenase-2 (COX-2) inhibition with celecoxib reduced blood pressure and inflammatory markers in obese rats.

Area of Science:

  • Biomedical Science
  • Cardiovascular Research
  • Obesity Studies

Background:

  • Monosodium glutamate (MSG) is known to induce obesity in animal models.
  • Obesity is associated with cardiovascular complications and inflammation.
  • The role of cyclooxygenase-2 (COX-2) in MSG-induced obesity-related pathologies requires further investigation.

Purpose of the Study:

  • To investigate the effect of COX-2 inhibition on cardiovascular and inflammatory markers in MSG-induced obese rats.
  • To determine the impact of celecoxib on blood pressure, heart rate, and inflammatory pathways in this model.

Main Methods:

  • Neonatal Wistar male rats were treated with MSG or saline.
  • Obese rats received celecoxib or saline from 60 to 90 days of age.
  • Cardiovascular parameters (MAP, HR) and biochemical markers (prostaglandins, nitric oxide, lipoperoxidation) were assessed.

Main Results:

  • MSG-induced obese rats exhibited hypertension (MAP=138±4 mmHg) compared to controls (MAP=118±2 mmHg).
  • Celecoxib treatment attenuated hypertension (MAP=126±2 mmHg) and reduced elevated plasma prostaglandins, COX-2 staining in cardiac tissue, and lipoperoxidation in obese rats.
  • MSG-induced liver steatosis was also ameliorated by celecoxib treatment.

Conclusions:

  • Increased blood pressure in MSG-obese rats is associated with elevated COX-2 products.
  • Prostaglandins likely play a significant role in the hypertensive and inflammatory aspects of MSG-induced obesity.
  • COX-2 inhibition may offer a therapeutic strategy for managing obesity-related cardiovascular and inflammatory conditions.