PHYTOCHEMICAL INVESTIGATION AND SCREENING FOR INFLAMMATORY BOWEL DISEASE ACTIVITY OF ETHANOLIC EXTRACT OF TECTONA GRANDIS LINN. BARK

Inflammatory bowel disease (IBD) is a multifactorial process that causes ulcerative colitis and Crohn’s disease due to unknown mechanisms associated with release of proinflammatory mediators. Aim of the present study is to evaluate inhibitory activity by bark extract Tectona grandis Linn. (TGE) against experimental induced IBD. Two different models were used to induce IBD viz., Indomethacin-induced enterocolitis and acetic acid induced ulcerative colitis in rats. Male wistar rats were pretreated with TGE the dose of 10 and 25 mg/kg p.o. daily for a period of 7 days. On 8^th and 9^th day indomethacin was administered (7.5 mg/kg, s.c.) for to induce enterocolitis. In case of acetic acid induced ulcerative colitis model, two ml (3%, v/v) acetic acid in saline was instilled into the rectum of a rat. Quantification of inflammation was done using myeloperoxidase assay (MPO), lactate dehydrogenase (LDH), lipid peroxidase (LPO). All parameters were altered in ulcerated rats, and improved in animals receiving TGE an effect that was comparable to that of the standard sulfasalazine, especially at the highest dose level. Evaluation based on macroscopic features showed significantly lower score values for drug treated and standard drug treated groups compared to the disease control groups. Histological examination of disease control group showed massive necrosis of the mucosa and submucosa. Drug treated group showed mild lesions, regeneration and inflammatory reaction. The sulfasalazine treated group showed suppressed inflammatory reaction. The results observed from MPO, LDH and LPO assays showed significant improvement of disease with extract treated groups compared to disease control group. Mechanism of action was determined by studying COX and prostaglandin inhibition studies. Results indicated that TGE shows inhibition of COX-1 is 42.35% and that of COX-2 is 45.8% and also produces action by inhibiting the synthesis of prostaglandin. The results obtained established the efficacy of the TGE against inflammatory bowel diseases possibly by its anti-inflammatory properties.