Influence of simultaneous inhibition of cyclooxygenase-2 and inducible nitric oxide synthase in experimental colitis in rats.

The inflamed mucosa in ulcerative colitis produces high amount of prostaglandin (PG) and nitric oxide (NO) through inducible enzymes: cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), respectively, implicating them as potential anti-inflammatory drug targets. COX-2 or iNOS-related treatments in different models of colitis have yielded ambiguous results ranging from exacerbation of disease to abolition of inflammation. iNOS and COX-2 induction is blocked by potent anti-inflammatory glucocorticoids, however, serious side effects including relapses limit their usefulness in colitis for long time. Simultaneous inhibition of iNOS and COX-2 was investigated in the current study in 2, 4, 6 trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats. Treatment group received rofecoxib, aminoguanidine hydrochloride or their combination at different doses at 48, 36, 24, 12 and 1 h prior to induction of colitis and 12 h later. Colonic myeloperoxidase (MPO), COX-2, nitrate and nitrite, tumor necrosis factor-alpha (TNF-alpha) and lipid peroxidation were maximally reduced by combination of 10 mg/kg rofecoxib and 30 mg/kg of aminoguanidine hydrochloride in TNBS-induced colitis in rats. However, maximum increase in SOD and catalase was noted by this combination. Rats treated with rofecoxib, aminoguanidine hydrochloride and their combinations reduced the inflammation, acute colonic damage produced by TNBS as verified by macroscopic changes in colon. Combination of rofecoxib (10 mg/kg) and aminoguanidine hydrochloride (30 mg/kg) has maximal protective effect on colonic injury induced by TNBS enema which is probably, via mechanism of local inhibition of iNOS and COX-2 activity in colonic mucosa and support the idea that simultaneous inhibition of iNOS and COX-2 inhibitors have a promising potential in the treatment of colitis.

Antinociceptive and antipyretic activities of Pongamia pinnata leaves.

In the present study, the antinociceptive activity of a 70% ethanol extract of Pongamia pinnata leaves (PLE) was investigated in different models of pain in mice and rats. Further, PLE was also evaluated for its antipyretic activity in Brewer's yeast-induced pyrexia in rats. Per os (p.o.) administration of the PLE (100-1000 mg/kg) produced significant antinociceptive activity in the hotplate and tail flick (central) as well as in acetic acid writhing and Randall-Selitto (peripheral) nociceptive tests suggesting the involvement of both central and peripheral mechanisms in alleviating the pain response. In addition, PLE also exhibited a significant antipyretic response in Brewer's yeast-induced pyrexia in rats. These results demonstrated that PLE possesses marked antinociceptive as well as antipyretic activities and thus scientifically validated its use in the treatment of pain and pyretic disorders.

Anti-inflammatory activity of Syzygium cumini bark.

The ethanolic extract of the bark of Syzygium cumini was investigated for its anti-inflammatory activity in animal models. The extract did not show any sign of toxicity up to a dose of 10.125 g/kg, p.o. in mice. Significant anti-inflammatory activity was observed in carrageenin (acute), kaolin-carrageenin (subacute), formaldehyde (subacute)-induced paw oedema and cotton pellet granuloma (chronic) tests in rats. The extract did not induce any gastric lesion in both acute and chronic ulcerogenic tests in rats. Thus, the present study demonstrated that S. cumini bark extract has a potent anti-inflammatory action against different phases of inflammation without any side effect on gastric mucosa.

In vitro anthelmintic action of some indigenous medicinal plants on Ascardia galli worms.

Different parts of ten indigenous medicinal plants were screened for their in vitro anthelmintic activity against Ascaridia galli worms of the birds. Preparations from Carica papaya, Sapindus trifoliatus, Butea frondosa and Momordica charantia were more effective than piperazine hexahydrate.