Cox-2 inhibition attenuates cardiovascular and inflammatory aspects in monosodium glutamate-induced obese rats.
OBJECTIVE
the purpose of the present work was to investigate the effect of cyclooxygenase-2 (COX-2) inhibition on the cardiovascular and inflammatory aspects promoted by monosodium glutamate (MSG)-induced obesity in rats.


METHODS
Neonatal Wistar male rats were injected with MSG (4 mg/g body weight ID) or equimolar saline (control). Treatment with celecoxib (50 mg/kg ip) or saline (0.9% NaCl ip) began at 60 days of age. At 90 days, all rats were anesthetized for catheterization of the femoral artery, and the mean arterial pressure (MAP) and heart rate (HR) were recorded once consciousness was regained.


RESULTS
MSG obese rats were hypertensive (MAP=138±4 mm Hg) compared with controls (MAP=118±2 mm Hg). After treatment with celecoxib, the hypertension was attenuated (MAP=126±2 mm Hg) in obese rats without changes in HR. The retroperitoneal and periepididymal fat weighed more in obese rats (Obese: Retro=7.08±0.51, Peri=6.36±0.81, CONTROL: Retro=3.60±0.46; Peri=3.24±0.42), but celecoxib did not alter these parameters. Plasma nitric oxide levels were not different between groups. However, the level of plasma prostaglandins, the immunohistochemical staining of COX-2 in cardiac tissue and plasma lipoperoxidation were higher in obese rats, and celecoxib attenuated these parameters. MSG produced liver steatosis that was also attenuated following celecoxib treatment.


CONCLUSIONS
Our data demonstrate an association between increased blood pressure and products of COX-2 in obese rats, suggesting a role for prostaglandins in the hypertensive and inflammatory aspects of MSG-induced obesity.
Cunha
N V
NV
Department of Physiological Sciences, State University of Londrina, Londrina, Paraná, Brazil.
de Abreu
S B
SB
Panis
C
C
Grassiolli
S
S
Guarnier
F A
FA
Cecchini
R
R
Mazzuco
T L
TL
Pinge-Filho
P
P
Martins-Pinge
M C
MC
D000273:Adipose Tissue / Q000473:pathology; D000818:Animals; D001769:Blood / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D000068579:Celecoxib; D051546:Cyclooxygenase 2 / Q000378:metabolism; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D015232:Dinoprostone / Q000097:blood; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D007249:Inflammation / Q000097:blood / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008054:Lipid Peroxides / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009566:Nitrates / Q000097:blood; D009765:Obesity / Q000139:chemically induced* / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D011720:Pyrazoles / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D012970:Sodium Glutamate / Q000494:pharmacology*; D013449:Sulfonamides / Q000494:pharmacology / Q000627:therapeutic use
D052246:Cyclooxygenase 2 Inhibitors; D008054:Lipid Peroxides; D009566:Nitrates; D011720:Pyrazoles; D013449:Sulfonamides; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D000068579:Celecoxib; D015232:Dinoprostone; D012970:Sodium Glutamate