Giris ve Amaç: Tümör nekroz faktör alfa, inflamatuvar barsak hastaligi patogenezinde önemli rol oynayan proinflamatuvar bir sitokindir. Pentoksifilin tümör nekroz faktör alfa’nin makrofajlardan salinimini inhibe etmektedir. Bu çalismada tümör nekroz faktör alfa inhibitörü pentoksifilin’nin siçanlarda asetik asit ile olusturulmus akut kolit ve trinitrobenzen sulfonik asit ile olusturulmus kronik kolit modelleri üzerine etkisi incelenmistir. Gereç ve Yöntem: Çalismada Swiss albino siçanlar randomize olarak onarli gruplara ayrilmistir. Asetik asit ile akut kolit veya trinitro-benzen sulfonik asit ile kronik kolit olusturulan siçanlara grup protokollerine göre intraperitoneal veya intrarektal pentoksifilin (100 mg/kg) koruyucu ya da tedavi edici sekilde uygulanmistir. Deney sonunda siçanlarda serum tümör nekroz faktör alfa, kolon myeloperoksidaz aktivitesi ve kolonun makroskopik, histolojik hasar skorlari incelenmistir. Bulgular: Pentoksifilin, asetik asit ile olusturulmus akut deneysel kolit modelinde kontrol grubu ile karsilastirildiginda makroskopik (1.33±0.28 ks 1.55±0.33) ve histolojik hasarda (3.11±0.20 ks 3.11±0.20) iyilesme saglamamistir. Ancak myeloperoksidaz aktivitesinde (0.689±0.021 ks. 1.358±0.121<0.0001) ve serum tümör nekroz faktör alfa seviyesinde (0.0344±0.020 ks. 13.03±3.278, <0.0001) belirgin düsüs gözlenmistir. Trinitro-benzen sulfonik asite bagli kronik kolit modelinde pentoksifilinin sistemik uygulamasi makroskopik hasarda iyilesme saglamistir (3.62±1.29 ks 6.90± .95, <0.05). Bu modelde tümör nekroz faktör alfa seviyeleri azalmakla birlikte fark anlamli bulunmami stir. Sonuç: Sonuç olarak akut ve kronik kolit modelinde koruyucu ya da tedavi edici sekilde pentoksifilin uygulamanin histopatolojik skorlar üzerine etkili olmadigini gördük. Kronik kolitte makroskopik hasardaki iyilesme tümör nekroz faktör alfa’dan bagimsizdir ve muhtemelen pentoksifilinin mikrosirkulasyonu düzeltmesi ile iliskilidir.
Background and Aims: Tumor necrosis factor-alpha is a proinflammatory cytokine that is also involved in the pathogenesis of colonic inflammation. Pentoxyphylline is a potent inhibitor of tumor necrosis factoralpha released by macrophages. The aim of this study was to investigate the effects of pentoxyphylline treatment in acetic acid-induced acute colitis and trinitrobenzene sulfonic acid-induced chronic colitis models in rats. Materials and Methods: Female Swiss Albino rats were randomly assigned into groups with 10 rats in each. Distal acute colitis was induced in rats by intracolonic instillation of acetic acid. trinitrobenzene sulfonic acid was used to induce chronic colitis. Pentoxyphylline 100 mg/kg was applied as IP or IR in relevant groups as pretreatment or treatment. Colonic damage was assessed by macroscopic and histological criteria as well as biochemical markers, including tissue myeloperoxidase activity and serum tumor necrosis factor-alpha levels. Results: Pentoxyphylline pretreatment did not affect the macroscopic (1.33±0.28 vs. 1.55±0.33) or microscopic (3.11±0.20 vs 3.11±0.20) histological scores in acute colitis. However, pentoxyphylline suppressed colonic myeloperoxidase activity (0.689±0.021 vs. 1.358±0.121<0.0001) and serum tumor necrosis factor-alpha levels (0.0344±0.020 vs.13.03±3.278, p<0.0001) significantly. Administration of pentoxyphylline to trinitrobenzene sulfonic acid-treated rats improved trinitrobenzene sulfonic acid-induced changes in macroscopy (3.62±1.29 vs. 6.90±0.95, p<0.05). Tumor necrosis factor- alpha levels were similar between pentoxyphylline-treated or -untreated trinitrobenzene sulfonic acid-induced colitis. Conclusions: In conclusion, pentoxyphylline systemically or locally applied in acute and chronic colitis does not affect colonic histopathological damage. Amelioration of macroscopic damage in trinitrobenzene sulfonic acid colitis with systemic pentoxyphylline treatment was most likely the result of improvement in microcirculation rather than changes in tumor necrosis factor-alpha levels.