Investigation of distribution of GSK-3beta signal pathway by age groups in cases of ulcerative colitis

Vol. 64 No. 1, 2023

ROMANIAN JOURNAL of MORPHOLOGY and EMBRYOLOGY

Caner Ozbey, Isil Aydemir

Ulcerative colitis (UC), one of the inflammatory bowel diseases, has been reported to increase in recent years. Although the exact cause is unknown, disruptions in the molecular pathways are thought to trigger UC. We aimed to examine the distributions of glycogen synthase kinase-3beta (GSK-3beta), nuclear factor-kappa B (NF-kappaB) and wingless/int-1 (Wnt-1) in different age groups diagnosed with UC. Patients diagnosed with UC were divided into four groups according to their ages: Group 1, aged 18-30 (n=20); Group 2, aged 31-45 (n=20); Group 3, aged 46-60 (n=20); Group 4, aged 61-75 (n=20). Tissue sections were histochemically stained to examine the parameters of epithelial cell height, length of crypt, thickness of muscularis mucosa and extent of submucosal fibrosis. The immunohistochemistry assay was performed using cell survival and for GSK-3beta, NF-kappaB and Wnt-1 cell growth markers. Immunoreactivities were evaluated using H-score and analyzed using the one-way analysis of variance (ANOVA) test for statistics. It was detected a decrease in the histopathological parameters whereas the immunoreactivities of GSK-3beta, NF-kappaB and Wnt-1 were increased with increasing age. The levels of GSK-3beta immunoreactivity were similar in both epithelium and submucosa in all groups. NF-kappaB immunoreactivity was higher in submucosa of Groups 1, 2 and 3, while Wnt-1 was enhanced in Groups 1 and 3. The results of histopathology showed that the integrity of the epithelial tissue in the colon deteriorated with increasing age. The expressions of GSK-3beta, NF-kappaB and Wnt-1 were detected in all age groups. We thought that there was a synergistic activation between these three markers. Nevertheless, studies are needed to investigate this molecular pathway.

Corresponding author: Isil Aydemir, Associate Professor, MD, PhD; e-mail: isil_aydemir@yahoo.com

DOI: 10.47162/RJME.64.1.07 Download PDF
Download cover
Download contents

Journal archive