Rat Model Of Pleurisy Research Articles

Peripheral blood mononuclear cells from rat model of pleurisy: The effects of hesperidin on ectoenzymes activity, apoptosis, cell cycle and reactive oxygen species production

The present study investigates the effect of hesperidin; a flavonone commonly found in citrus fruits, on the ectoenzymes (ectonucleotidase and ecto-adenosine deaminase) activity, cell viability, apoptosis, cell cycle arrest and reactive oxygen species production in peripheral blood mononuclear cells (PBMCs) from rat model of pleurisy. Wistar rats were pretreated with either saline or hesperidin (80mg/kg) by oral gavage for 21days and injected intrapleurally with 2% carrageenan or saline on the 22nd day. PBMCs were subsequently prepared after 4h of carrageenan induction. The results revealed that hesperidin may exhibit its anti-inflammatory effects through possible modulation of ectonucleotidase (E-NTPDase) and ecto-adenosine deaminase (E-ADA) activities, reduction of intracellular reactive oxygen species, prevention of DNA damage and modulation of apoptosis as well as activation of cell cycle arrest. This study suggests some possible underlying anti-inflammatory mechanisms of hesperidin on PBMCs in acute inflammatory condition. Furthermore, hesperidin may minimize oxidative injury mediated pleurisy in rat.

Effect of the selective COX-2 inhibitors, celecoxib and rofecoxib in rat acute models of inflammation.

This study evaluates the action of celecoxib and rofecoxib, two selective cyclooxygenase-2 (COX-2) inhibitors in two acute models of inflammation, carrageenan (Cg)-induced rat pleurisy, and paw oedema formation. Male Wistar rats (N = 4-10 per group) were used. A fixed volume of PBS or carrageenan was injected into the pleural cavity or into the paw. Furthermore, the myeloperoxidase (MPO) activity and the levels of nitrite/nitrate (NOx), interleukin-1beta (IL-1beta), tumor necrosis factor-a (TNF-a) and PGE2 were also assessed in the paw tissue or in pleural exudate. Dexamethasone (DEX, 0.5 mg kg(-1), s.c., -4 h) and indomethacin (INDO, 3 mg kg(-1), p.o., -1 h) suppressed Cg-induced pleural exudate accumulation by 84 and 77% and inflammatory cell influx by 66 and 47%, respectively. In contrast, celecoxib (CLX, 10 mg kg(-1), p.o., -1 h) or rofecoxib (RFX, 10 mg kg(-1) , p.o., -1 h) only reduced the Cg-induced pleural exudate volume by 44 and 40%, respectively, but had no significant effect over inflammatory cell influx. At the same doses used for pleurisy, DEX, INDO, CLX, RFX and SC-560 (a selective COX-1 inhibitor, 40 mg kg(-1), p.o., -1 h), inhibited the Cg-induced paw oedema by 49, 31, 21, 21 and 17%. DEX, INDO or SC-560 reduced the level of MPO by 71, 78 and 59%, while CLX or RFX produced a small, but significant increase (28 or 16%) in MPO activity. In the rat model of pleurisy, PGE2 levels in cell-free exudates were significantly attenuated by 91, 89, 57 and 65% in animals treated with DEX, INDO, CLX or RFX. In contrast, INDO reduced significantly the whole bloodTXB, synthesis (59%) while DEX and INDO reduced the pleural content of NOx significantly. Treatment of animals with CLX or RFX did not alter the content of pro-inflammatory cytokines IL-1beta or TNF-alpha in the pleural exudate, but CLX reduced IL-1beta levels in the rat paw tissue and RFX increased TNF-alpha in this tissue. Together these results provide consistent evidence indicating that the selective COX-2 inhibitors CLX and RFX, in contrast to DEX, INDO or SC-560, despite reducing greatly the Cg-induced pleural exudation, PGE2 content and paw oedema have only partial acute anti-inflammatory properties in two different rat acute models of inflammation.