Digestive diseases and sciences · 2008
The effects of caffeic acid phenethyl ester (CAPE) on TNBS-induced colitis in ovariectomized rats.
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Ek Rauf Onur, Serter Mukadder, Ergin Kemal, Yildiz Yuksel, Cecen Serpil, Kavak Tulay, Yenisey Cigdem
Аннотация
AIM: The aim of this investigation was to examine the effects of caffeic acid phenethyl ester (CAPE) on the development of colitis and antioxidant parameters in bilateral ovariectomized rats subjected to trinitrobenzene sulfonic acid (TNBS)-induced colitis.
MATERIALS AND METHODS: Twenty-one Wistar Albino ovariectomized female rats were divided into four subgroups (n = 5 or 6) (colitis control, vehicle control, CAPE 10 and 30 mg/kg, respectively). Colitis was induced using an enema of TNBS and ethanol, following which CAPE was administrated for 3 days to induce colitis and effect of CAPE was subsequently evaluated.
RESULTS: Based on microscopic damage scores, there was no difference between rats of the TNBS-colitis and the vehicle-treated groups, whereas treatment with CAPE 10 and 30 mg/kg, respectively, caused a significant reduction in colon injury compared to that observed in rats of the TNBS-colitis and vehicle-treated groups. The histologies of both treatment groups were not significantly different. In terms of the biochemical analyses, myeloperoxidase levels in rats from the CAPE 10 and 30 mg/kg groups were significantly different from that of the colitis control rats; however, the levels of malondialdehyde (MDA), catalase and reduced glutathione (GSH) were only significantly different from the levels found colitis control rats in rats administered 10 mg/kg. The levels of MDA, GSH and SOD in rats given CAPE were also significantly different from those of rats in the vehicle control group. These results were consistent with histological findings.
CONCLUSION: CAPE may have a positive effect on the inflammatory bowel disease treatment process and could, therefore, be used as an adjunct therapy in colitis. These effects of CAPE may occur through antiinflammatory and antioxidant mechanisms.
MATERIALS AND METHODS: Twenty-one Wistar Albino ovariectomized female rats were divided into four subgroups (n = 5 or 6) (colitis control, vehicle control, CAPE 10 and 30 mg/kg, respectively). Colitis was induced using an enema of TNBS and ethanol, following which CAPE was administrated for 3 days to induce colitis and effect of CAPE was subsequently evaluated.
RESULTS: Based on microscopic damage scores, there was no difference between rats of the TNBS-colitis and the vehicle-treated groups, whereas treatment with CAPE 10 and 30 mg/kg, respectively, caused a significant reduction in colon injury compared to that observed in rats of the TNBS-colitis and vehicle-treated groups. The histologies of both treatment groups were not significantly different. In terms of the biochemical analyses, myeloperoxidase levels in rats from the CAPE 10 and 30 mg/kg groups were significantly different from that of the colitis control rats; however, the levels of malondialdehyde (MDA), catalase and reduced glutathione (GSH) were only significantly different from the levels found colitis control rats in rats administered 10 mg/kg. The levels of MDA, GSH and SOD in rats given CAPE were also significantly different from those of rats in the vehicle control group. These results were consistent with histological findings.
CONCLUSION: CAPE may have a positive effect on the inflammatory bowel disease treatment process and could, therefore, be used as an adjunct therapy in colitis. These effects of CAPE may occur through antiinflammatory and antioxidant mechanisms.