Original Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Mar 7, 2011; 17(9): 1135-1142
Published online Mar 7, 2011. doi: 10.3748/wjg.v17.i9.1135
Octreotide ameliorates gastric lesions in chronically mild stressed rats
Noha N Nassar, Mona F Schaalan, Hala F Zaki, Dalaal M Abdallah
Noha N Nassar, Hala F Zaki, Dalaal M Abdallah, Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt
Mona F Schaalan, Department of Biochemistry, Faculty of Pharmacy, Misr International University, Cairo 11135, Egypt
Author contributions: All authors contributed equally to conception, design, acquisition and analysis of data. Similarly, all authors contributed equally to drafting the article or revising it critically for important intellectual content and final approval of the version to be published.
Correspondence to: Dr. Dalaal M Abdallah, PhD, Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. mohamed.alaa@bms.com
Telephone: +20-2-23632245 Fax: +20-2-23628246
Received: October 18, 2010
Revised: January 10, 2011
Accepted: January 17, 2011
Published online: March 7, 2011
Abstract

AIM: To evaluate the effect of chronic mild stress (CMS) on the emergence of gastric ulcers and possible modulation by octreotide, a synthetic somatostatin analogue.

METHODS: Adult male Wistar rats were subjected to nine different unpredictable random stress procedures for 21 d, a multifactorial interactional animal model for CMS. Octreotide was administered daily for 21 d at two dose levels (50 and 90 μg/kg) before exposure to stress procedure. Macro- and microscopical assessments were made, in addition to quantification of plasma corticosterone and gastric mucosal inflammatory, oxidative stress, and apoptotic biomarkers.

RESULTS: Exposure to CMS elevated plasma corticosterone (28.3 ± 0.6 μg/dL, P = 0.002), an event that was accompanied by gastric lesions (6.4 ± 0.16 mm, P = 0.01) and confirmed histopathologically. Moreover, the insult elevated gastric mucosal lipid peroxides (13 ± 0.5 nmol/g tissue, P = 0.001), tumor necrosis factor-α (3008.6 ± 78.18 pg/g tissue, P < 0.001), prostaglandin E2 (117.1 ± 4.31 pg/g tissue, P = 0.002), and caspase-3 activity (2.4 ± 0.14 OD/mg protein, P = 0.002). Conversely, CMS mitigated interleukin-10 (627.9 ± 12.82 pg/g tissue, P = 0.001). Furthermore, in animals exposed to CMS, octreotide restored plasma corticosterone (61% and 71% from CMS, P = 0.002) at both dose levels. These beneficial effects were associated with a remarkable suppression of gastric lesions (38% and 9% from CMS, P = 0.01) and reversal of derangements in gastric mucosa.

CONCLUSION: The current investigation provides evidence that exposure to CMS induces gastric ulceration, which was alleviated by administration of octreotide possibly possessing antioxidant, anti-inflammatory, and anti-apoptotic actions.

Keywords: Gastric ulcer; Chronic mild stress; Octreotide; Inflammation; Oxidative stress; Apoptosis; Histopathology