English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The peroxisome proliferator-activated receptors (PPARs) have been implicated in the regulation of endothelial cell inflammatory response. The purpose of the present study was to clarify the molecular mechanism of NSAIDs in controlling inflammation regarding the gene expression of PPARα and PPARγ1 in a rat model of chronic inflammation. Wistar rats were classified into 5 experimental groups; 9 rats each. Group (1) normal control; group (2) injected s.c. with 0.3 % carrageenan in muscle on days 1, 4 and 7. Groups (3, 4 and 5) were injected s.c. with carrageenan and at the same time given orally 10 mg/Kg Celecoxib, 12.5 mg/Kg Nimesulide or 10 mg/Kg sulindac, respectively. On day 7, edema was measured before scarification. Gene expression PPARγ1 and PPARα was measured in rat muscle by RT-PCR. COX-2 was analyzed in rat muscle by ELISA. Celecoxib produced the greatest % inhibition of carrageenan-induced edema. PPARγ1 and PPARα gene expression were significantly increased by NSAIDs treatment compared with carrageenan-untreated group. The inhibition of COX-2 together with upregulation of PPAR and PPARγ1 nominate NSAIDs to be promising candidates for pharmacologic treatment of tumorgenesis.

iosr journal of pharmacy and biological sciences

Gene Expression of Peroxisome Proliferator-Activated Receptor Is Upregulated by Nonsteroidal Anti-Inflammatory Drugs and Correlates with Cyclooxygenase-2 Suppression In Inflamed-Rat Muscle