Effect of anti-inflammatory drugs on pleurisy induced by latex of Calotropis procera in rats.

In present study, we have characterized the inflammation induced by latex of Calotropis procera in the rat pleurisy model and evaluated the effect of various inhibitors of inflammatory mediators. Injection of dried latex (DL) into the pleural cavity elicited an acute inflammatory response characterized by protein rich fluid accumulation and leucocyte (polymorphonuclear cells, and mononuclear cells) infiltration in the pleural cavity. The peak inflammatory response was obtained at 6h when the fluid volume, protein concentration and cell infiltration were maximum. All these parameters were attenuated by phenylbutazone (PBZ), celecoxib, dexamethasone, cyproheptadine and chlorpheniramine. All these drugs were also effective in inhibiting the production of prostaglandin E(2) (PGE(2)). Of all the drugs tested, dexamethasone was most effective in inhibiting DL induced pleurisy. The results clearly indicate that prostaglandins (PGs) and biogenic amines play a key role in the development of pleurisy induced by DL and it serves as a model to evaluate drugs inhibiting cellular influx associated with inflammatory response.

Involvement of prostaglandins in inflammation induced by latex of Calotropis procera.

INTRODUCTION: The aerial parts of the plant Calotropis procera produce milky white latex that causes inflammation of the skin and mucous membranes. Prostaglandins are one of the mediators released in an inflammatory response following induction of cyclooxygenase (COX). In the present study, we have evaluated the role of prostaglandins in inflammatory response elicited by the latex of C. procera. METHODS: Aqueous extract of dried latex of C. procera was injected into the 6-day air-pouch in the rat. The inflammatory response was evaluated by studying the air-pouch fluid for its volume, protein and prostaglandin (PG) E2 concentrations, and leucocyte counts. The granulation tissue from the pouch was quantified and studied for COX-2 expression by reverse transcriptase-polymerase chain reaction. The inhibitory effect of celecoxib and dexamethasone was evaluated on the aforementioned parameters. RESULTS: Dried latex produced an inflammatory response that was maximum at 6 h. It was associated with the accumulation of protein-rich fluid, leucocytes and PGE2 production. It also resulted in granulation of the pouch cavity that was a maximum on day 3. COX-2 expression could be detected in the granulation tissue on day 1 and it increased progressively up to day 5. The anti-inflammatory drugs celecoxib and dexamethasone significantly attenuated the inflammatory response and inhibited COX-2 expression in granulation tissue. CONCLUSIONS: Latex of C. procera induces an inflammatory response characterized by an early exudative phase accompanied by PGE2 production and a late proliferative phase associated with COX-2 induction. Both the phases were effectively inhibited by COX-2 inhibitors.

Histamine mediates the pro-inflammatory effect of latex of Calotropis procera in rats.

INTRODUCTION: Calotropis procera is known to produce contact dermatitis and the latex of this plant produces intense inflammation when injected locally. However, the precise mode of its pro-inflammatory effect is not known. In present study we have pharmacologically characterized the inflammation induced by latex of C. procera in a rat paw edema model and determined the role of histamine in latex-induced inflammation. METHODS: Inflammation was induced in the hind paw of rats by injecting different doses of dried latex (DL) of C. procera. The inhibitory effect of phenylbutazone, dexamethasone, celecoxib, cyproheptadine, chlorpheniramine and compound 48/80 on edema volume was evaluated and compared with that against carrageenan. The histamine content of DL was measured fluorometrically. RESULTS: DL produced dose-dependent inflammation of the rat paw. Cyproheptadine and chlorpheniramine effectively inhibited DL-induced inflammation (90%; p < 0.01), while anti-inflammatory drugs phenylbutazone, dexamethasone and celecoxib were more effective against carrageenan-induced inflammation. Depletion of mast cell histamine by compound 48/80 produced a significant decrease in DL-induced inflammation as compared with carrageenan (500% versus 25%). DL was also found to contain about 6 microg/g of histamine. CONCLUSIONS: Thus, our study shows that the biogenic amines play a significant role in C. procera latex-induced inflammation and antihistaminic drugs could be effectively used to inhibit inflammatory response elicited by exposure to latex.