Oral Presentation - 105
Intestinal Adaptation and Endoplasmic Reticulum Stress in A Rat Model of Short Bowel Syndrome
Selin Ural 1, Esma Kırımlıoğlu 2, Güngör Karagüzel 1
1 Akdeniz University Hospital, Faculty of Medicine, Department of Pediatric Surgery, Antalya, Turkey
2 Akdeniz University School of Medicine, Department of Histology and Embryology, Antalya, TURKEY
Purpose: The etiopathogenesis of intestinal adaptation following massive small bowel resection (MSBR) remains unclear. This study investigates the role of endoplasmic reticulum stress (ERS) in intestinal adaptation in a rat model of small bowel syndrome (SBS) based on MSBR.
Method:
Seventy Wistar rats were assigned to control (C, n=10), sham (S, n=30), and resection (R, n=30) groups. Group R underwent 75% MSBR to establish an SBS model. Groups S and R rats were sacrificed on days 3, 9 and 15 to reveal changes in acute, early adaptive and maintenance phases, respectively. Immunohistochemical expressions of GRP78 and CHOP as ERS markers were evaluated in the jejunum and ileum segments.
Results: Jejunal GRP78 expression in Group R was significantly increased in all phases compared to Groups C and S. Ileal GRP78 expression in Group R was significantly increased only on day 9, but there were insignificant increases on days 3 and 15 compared to Groups C and S. In all adaptation phases, there was a gradual increase in jejunal CHOP expressions in Group R, while there was a gradual decrease in Group S. Ileal CHOP expressions of Group R were significantly increased on day 9 compared to days 3 and 15. However, ileal CHOP expressions between Group R and Group S revealed very mixed results
Conclusions: This study demonstrates that MSBR induces segment-specific and ERS marker-specific modulation of ERS during intestinal adaptation. Sustained upregulation of GRP78 in the jejunum suggests a supportive role in epithelial remodeling throughout all phases of adaptation. In contrast, suppression of CHOP expression—particularly in early phases—indicates that MSBR may attenuate pro-apoptotic ERS signaling to facilitate adaptation. These findings highlight a dual and dynamic involvement of ERS in post-resection adaptation and support further exploration for a potential therapeutic strategy in SBS.