Elife ERARSLAN, Cansel TÜRKAY, Burak UZ, Arif KAYA, Cemile KOCA, Reyhan BAYRAK, Özlem ALICI

The effects of caffeic acid phenethyl ester (CAPE) on acetic acid induced colitis in rats

Kafeik asit fenetil ester (KAPE), iskemi-reperfüzyon ve toksik hasarda oksidatif stres yoluyla ortaya çıkan reaktif oksijen ürünlerinden dokuyu koruyan, propolis ekstresinin aktif bir komponentidir. İnflamatuar barsak hastalığının (İBH) patogenezinde anormal oksidatif metabolizma önemli olduğundan, İBH’da serbest radikallerin rolü üzerine dikkat çekilmiştir. Bu çalışmanın amacı ratlarda asetik asitin (AA) neden olduğu kolitte KAPE’nin antioksidan parametrelere ve kolit gelişimi üzerine etkilerin değerlendirmektir. 21 adet 150-200 g ağırlığında Wistaralbino dişi rat kullanıldı. Ratlar rastgele 3 gruba ayrıldı: sırasıyla kontrol grubu (6), kolit grubu (8) ve KAPE grubu (7). %4’lük AA kolon içine lavmanla verilerek kolit oluşturuldu. AA lavmanıyla kolit oluşturulduktan sonra 3 gün süreyle KAPE verilerek kolit üzerine KAPE’nin sonrak etkileri değerlendirildi. Kolit grubunda artmış olan kolonik malondialdehit ve nitrik oksit düzeyi KAPE tedavisiyle (10 µmol/kg) azaldı (sırasıyla p=0.043, p=0.006). Kolit grubunda azalmış olan glutatyon aktivitesi KAPE tedavisiyle arttı (p=0.008). KAPE makroskobik olarak kolit grubunun lezyon skorunda azalmaya neden olmadı (p>0.05). Bizim verilerimiz KAPE tedavisinin biyokimyasal parametrelerde pozitif etkisini gösterirken, istatistiksel olarak anlamlı bir histolojik iyileşme oluşturmadığını göstermiştir. KAPE, antioksidan ve antiinflamatuar etkileriyle ratlarda AA ile oluşturulan kolit modelinde yararlı gibi görünmektedir. Biz daha uzun süreli ve daha yüksek doz KAPE ile yapılan ilave, daha anlaşılır deneysel çalışmalarla KAPE’nin etkilerinin değerlendirilmes gerektiğine inanıyoruz.

Kafeik asit fenetil esterin ratlarda asetik asitle indüklenmiş kolite etkileri

Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, protects tissues from reactive oxygene species mediated oxidative stress in ischemia-reperfusion and toxic injuries. Since abnormal oxidative metabolism is important in the pathogenesis of inflammatory bowel disease (IBD), increased attention has been focused on the role of free radicals in IBD. The aim of this study was to investigate the effect of CAPE on the development of colitis and antioxidant parameters of rats subjected to acetic acid (AA) induced colitis. Twenty one female Wistar-albino rats weighing 150-200 g were used. The rats were randomly divided into three groups: control group (n=6), colitis group (n=8), CAPE group (n=7), respectively. Colitis was induced by intracolonic enema with 4% AA. Colitis was induced using an enema of AA following which CAPE was administrated for 3 days to induce colitis and effect of CAPE was subsequently evaluated. The increase in colonic malondialdehyde and nitric oxide level at the colitis group was reduced by CAPE (10 µmol/kg) treatment (p=0.043, p=0.006, respectively). Reduced glutathione activity in the colitis group was increased by CAPE treatment (p=0.008). Treatment with CAPE did not reduce the lesion score of the colitis group at macroscopic level (p>0.05). Our data showed its positive effects on biochemical parameters, although there was not statistically significant histologic improvement with CAPE tratment. CAPE seemed to be beneficial in an AA-induced rat colitis model through the antioxidant and anti-inflammatory effect. We believe further studies such as longer CAPE treatment and higher dosages are needed to investigate the effects of CAPE more clearly in experimental colitis.

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