Suppressive effect of COX2 inhibitor on the progression of adipose inflammation in high-fat-induced obese rats.

Abstract:

BACKGROUND:The aim was to examine whether the inhibition of selective cyclooxygenase (COX) 2 activation could suppress the development of inflammatory reaction in visceral and subcutaneous abdominal fats of high-fat-induced obese rats. MATERIALS AND METHODS:The rats were fed separately regular diet (CONT), high-fat diet ad libitum or energy-restrictedly (HFr) for 12 weeks. Rats fed high-fat diet ad libitum were further divided into those co-treated with vehicle (HFa), a selective COX2 inhibitor-celecoxib (HFa-Cel) or nimesulide (HFa-Nim). Oral glucose tolerance test (OGTT) was performed at the end of weeks 4, 8, 12. Another set of rats with similar grouping was divided into those with a 4-, 8- or 12-week intervention for tissue sampling. RESULTS:Body and epididymal fat weights were increased similarly in HFa, HFa-Cel and HFa-Nim. Time-dependent increases in plasma insulin, triglyceride, impaired OGTT shown in HFa were significantly reversed in HFa-Cel and HFa-Nim. The obese-linked increases in gene expressions of COX-2, monocyte chemoattractant protein-1 (MCP-1) and tumour necrosis factor-alpha (TNF-alpha) in epididymal and subcutaneous fats (especially in the former) were significantly suppressed in HFa-Cel and HFa-Nim. The protein contents of MCP-1 and TNF-alpha in epididymal fats were changed consistently with their gene expressions. Plasma MCP-1 was increased time-dependently in HFa and suppressed in HFa-Cel and HFa-Nim. The increased CD68 positive cells showed in both epididymal and subcutaneous fats of HFa were significantly attenuated in HFa-Cel and HFa-Nim. CONCLUSIONS:Our findings suggest that COX2 activation is crucially involved in the development of inflammatory response in adipose tissues of high-fat-induced obese rats.

journal_name

Eur J Clin Invest

authors

Hsieh PS,Lu KC,Chiang CF,Chen CH

doi

10.1111/j.1365-2362.2009.02239.x

subject

Has Abstract

pub_date

2010-02-01 00:00:00

pages

164-71

issue

2

eissn

0014-2972

issn

1365-2362

pii

ECI2239

journal_volume

40

pub_type

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