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Indian Journal of Pharmacology, Vol. 36, No. 3, June, 2004, pp. 177-178 Research Letter Influence of sodium curcuminate on castor oil-induced diarrhea in rats Gnanasekar N, Perianayagam JB Faculty of Pharmaceutical Sciences, Guru Jambheshwar University, Hisar Code Number: ph04060 Sir, The rhizome of Curcuma longa Linn. (turmeric) is widely used in the Indian system of medicine. Curcumin (diferuloyl methane) isolated from the alcoholic extract of turmeric has been shown to be a potent antiinflammatory agent.[1] The sodium salt of curcumin was found to be more effective in inhibiting carrageenin-induced rat hind paw edema when compared with curcumin and some of its semi-synthetic analogues.[2] It has also been reported that sodium curcuminate decreased the resting tone of rabbit intestine and reversibly inhibited contractions induced by nicotine, acetylcholine, 5-hydroxy tryptamine, histamine and barium chloride on isolated guinea pig ileum.[3] Drugs possessing antiinflammatory activity have been shown to delay castor oil-induced diarrhea, suggesting the involvement of prostaglandins in this mechanism.[4] The antiinflammatory action of sodium curcuminate is not fully understood. Therefore, the present study was designed to investigate the mechanism that might account for the antiinflammatory action of sodium curcuminate by castor oil-induced diarrhea in rats. The sodium salt of curcumin (Loba chemie) was prepared as described earlier[1] and used in the study. The experimental study was approved by the Institutional Animal Ethics Committee. A modification of the method of Awounters et al.[4] was followed. In this study, Albino rats (Wistar) of either sex (200-260 g) were fasted for 18 h and water was provided ad libitum. The animals were divided into six groups of six animals each. Sodium curcuminate was administered (0.1, 0.2, 0.6 and 1 mg/kg) orally to the first four groups. The fifth group received the standard antiinflammatory agent, indomethacin (10 mg/kg, i.p.) and the sixth group water (vehicle control). One hour after treatment, each animal received 1 ml of castor oil (CDH, Mumbai) orally by gavage and was then observed for defecation. The rats were observed over a 4 h period for the assessment of characteristic diarrhea droppings in the transparent plastic dishes placed beneath the individual rat cages. The data were analyzed by one-way analysis of variance, followed by Dunnett′s test and P<0.05 was considered significant. Administration of castor oil produced characteristic semisolid diarrhea droppings in 18 h starved rats of the control group during the 4 h observation period [Table - 1]. Sodium curcuminate dose-dependently inhibited the occurrence of diarrhea as compared to the vehicle-treated control rats. The highest dose of sodium curcuminate (1 mg/kg) significantly inhibited castor oil-induced diarrhea with the percentage inhibition of 80.03, which was comparable to that of indomethacin (10 mg/kg). The delay of castor oil-induced diarrhea has been demonstrated to characterize non-steroidal antiinflammatory drugs (NSAIDs). Awounters et al[4] tested 44 NSAIDs and found that the selective potencies of the drugs in castor oil-induced diarrhea and in the carrageenin-induced test correlated well. The sodium curcuminate was found to be more effective in inhibiting carrageenin-induced rat paw edema when compared with curcumin and some of its semisynthetic analogues.[2] The delay of castor oil-induced diarrhea and the inhibition of carrageenin induced inflammation by sodium curcuminate may be related to the inhibition of prostaglandin synthesis. In earlier studies, sodium curcuminate has been shown to antagonize the contractions of isolated guinea pig ileum induced by various agonists.[3] This property is also shared by most of the NSAIDs.[5] The inherent resting tone of the intestinal smooth muscle is known to be maintained by continuous intramural generation of prostaglandins and the inhibition of prostaglandin biosynthesis by NSAIDs results in decrease of the resting tone.[6] Sodium curcuminate has been shown to produce a similar decrease in the resting tone of rabbit intestine.[3] Hence, it may be quite possible that all these activities could be attributed, at least partly, to inhibition of prostaglandin biosynthesis. However, further studies are required to understand the mechanism that might account for the antiinflammatory and related action of sodium curcuminate. REFERENCES
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