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dc.contributor.authorTopal, Cumhur
dc.contributor.authorUzun, Hafize
dc.contributor.authorAhmad, Sarfraz
dc.contributor.authorAktas, Serife
dc.contributor.authorKABASAKAL, LEVENT
dc.contributor.authorOzel, Yahya
dc.contributor.authorElcioglu, H. Kubra
dc.contributor.authorCevikelli, Z. Ayca
dc.contributor.authorKudas, Ilyas
dc.date.accessioned2021-03-05T13:20:07Z
dc.date.available2021-03-05T13:20:07Z
dc.identifier.citationOzel Y., Elcioglu H. K. , Cevikelli Z. A. , Kudas I., Ahmad S., Uzun H., Topal C., Aktas S., KABASAKAL L., "Ischemic colitis of the colon in streptozotocin-induced diabetic rats", MOLECULAR AND CELLULAR BIOCHEMISTRY, cilt.439, ss.87-93, 2018
dc.identifier.issn0300-8177
dc.identifier.othervv_1032021
dc.identifier.otherav_b1bff168-a84e-404f-82ff-7a1e5fc2d6e4
dc.identifier.urihttp://hdl.handle.net/20.500.12627/118403
dc.identifier.urihttps://doi.org/10.1007/s11010-017-3138-2
dc.description.abstractThis study focuses on two inflammatory diseases, viz., "diabetes mellitus (DM)" that causes serious complications such as retinopathy, nephropathy, and neuropathy, and "ischemic colitis" which is evoked by DM. Ischemic colitis originates from the reduction in mesenteric blood flow to the colon with existence of the occlusive or non-occlusive reasons. Our study objective was to provide early diagnostic approach for ischemic colitis in streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley rats were divided into four groups: (i) control use of 0.1 M citrate buffer, the solvent of streptozotocin (C), (ii). induced ischemia (I), (iii) rats subjected to 60 mg/kg STZ intraperitoneally to induce type 1 diabetes (D) (48 h after STZ injection, blood glucose levels >200 mg/dl were considered as diabetic), and (iv) diabetic rats subjected to intestinal ischemia (D+I). The third diabetic group (D) was not operated. At the end of the experimental period, rats were sacrificed, C-reactive protein (CRP) and calprotectin levels were measured in the serum and colon tissue specimens. Tissue specimens were also analyzed histologically. We found that serum and colon calprotectin levels were elevated in the D+I group compared to the D and/or I group alone, but relatively calprotectin levels increased in I as compared to C group in colon tissues. CRP levels were significantly increased with ischemic colitis in diabetes, while colon CRP levels were decreased. These results provide evidence for the existence of inflammation in the STZ-induced diabetic rats with ischemic colitis. In conclusion, our measurements of serum calprotectin levels of STZ-induced diabetic rats with ischemic colitis provide a practical approach for an early diagnosis of ischemic colitis. Furthermore, these biochemical analyses correlate well with the histopathologic findings of STZ-induced diabetic rats with ischemic colitis. Future studies would be desirable to further strengthen the role of calprotectin in the early diagnosis of ischemic colitis in diabetics clinical settings.
dc.language.isoeng
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectTemel Bilimler
dc.subjectTemel Tıp Bilimleri
dc.subjectHistoloji-Embriyoloji
dc.subjectSağlık Bilimleri
dc.subjectTıp
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectHÜCRE BİYOLOJİSİ
dc.titleIschemic colitis of the colon in streptozotocin-induced diabetic rats
dc.typeMakale
dc.relation.journalMOLECULAR AND CELLULAR BIOCHEMISTRY
dc.contributor.departmentIstanbul Umraniye Training & Research Hospital , ,
dc.identifier.volume439
dc.identifier.startpage87
dc.identifier.endpage93
dc.contributor.firstauthorID251379


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