Thyroid hormones increase stomach goblet cell numbers and mucin expression during indomethacin induced ulcer healing in Wistar rats

Abstract

BackgroundGastric ulcers are mucosal discontinuities that may extend into the mucosa, submucosa or even deeper. They result from an imbalance between mucosal aggressors and protective mechanisms that include the mucus bicarbonate layer. Thyroid hormones have been shown to accelerate gastric ulcer healing in part by increasing the adherent mucus levels. However, the effects of thyroid hormones on goblet cell numbers and expression of neutral and acidic mucins during ulcer healing have not been investigated.MethodsThirty six adult male Wistar rats were randomly divided into six groups each with six animals. Group 1 (normal control) and group 2 (negative control) were given normal saline for eight weeks. Groups 3 and 4 were given 100 μg/kg per day per os of thyroxine so as to induce hyperthyroidism. Groups 5 and 6 received 0.01% (w/v) Propylthiouracil (PTU) for 8 weeks so as to induce hypothyroidism. After thyroid hormonal levels were confirmed using radioimmunoassay and immunoradiometric assays, ulcer induction was done using 40 mg/kg intragastric single dose of Indomethacin in groups 2, 3 and 5. Stomachs were extracted after day 3 and 7 of ulcer induction for histological examination. Histochemistry was carried out using Periodic Acid Shiff and Alcian Blue. The number of acidic and neutral goblet cells were determined by counting numbers per field. Mucin expression (%) was determined using Quick Photo Industrial software version 3.1.ResultsThe numbers of neutral goblet cells (cells/field) increased significantly (P < 0.05) in the ulcer+thyroxine (14.67 ± 0.33), thyroxine (17.04 ± 1.71) and ulcer+PTU (12.89 ± 1.06) groups compared to the normal control (10.78 ± 1.07) at day 3. For the acidic goblet cells, differences between treatment groups were more pronounced at day 7 between the ulcer+thyroxine (22.56 ± 1.26) and thyroxine (22.89 ± 0.80). We further showed that percentage expression of both neutral and acidic mucins was significantly higher in the ulcer+thyroxine (9.23 ± 0.17 and 6.57 ± 0.35 respectively) and thyroxine groups (9.66 ± 0.21 and 6.33 ± 0.38 respectively) as compared to the normal control group (4.08 ± 0.20 and 4.38 ± 0.11 respectively) at day 3 after ulcer induction.ConclusionThis study confirms the role played by thyroid hormones in healing of indomethacin induced gastric ulcers. The study further demonstrates increased numbers of both neutral and acidic goblet cells and the increase in expression of both neutral and acidic mucins during healing of indomethacin induced ulcers.Electronic supplementary materialThe online version of this article (10.1186/s13044-018-0050-0) contains supplementary material, which is available to authorized users.

Ethanol-induced gastric ulcer in rats and intervention of tert-butylhydroquinone: Involvement of Nrf2/HO-1 signalling pathway

“…Namulema et al reported the reduction in the number of goblet cells in ethanol-exposed rats. 48 IHC staining revealed the increased expression of phospho-NF-kB p65 and COX-2 in ethanol-exposed stomach in comparison to control. While preadministration of tBHQ at both the doses significantly reduced the expression of p-NF-kB p65 and COX-2 in comparison to the ulcer group.…”

Unique Novel Role of Adropin in a Gastric Ulcer in a Rotenone-Induced Rat Model of Parkinson’s Disease

“…rotenone injection (2.5 mg/kg, daily) dissolved in 98% PEG-400 and 2% DMSO, 35,36 the ulcer induction was done, after an overnight fast but with access to water, using a single intragastric indomethacin (IND; Liometacen) dose by oral gavage (40 mg/kg) dissolved in distilled water. 36 Adropin Treated PD/Ulcer Group (15 Rats, Group III). Adropin 34−76 was dissolved in distilled water and administered in a dose of 2.1 μg/kg/ day (i.p.)…”

Tormentic acid, a triterpenoid isolated from the fruits of Chaenomeles speciose , protected indomethacin-induced gastric mucosal lesion via modulating miR-139 and the CXCR4/CXCL12/PLC/PKC/Rho a/MLC pathway

“…With the change in modern lifestyles, environmental pollution, and irrational use of non-steroidal anti-inflammatory drugs (NSAIDs), gastrointestinal mucosal lesions have become one of the major diseases that seriously endanger public health and social development, causing great economic and social burdens worldwide, especially in developing countries (O’Malley 2003 ; Namulema et al. 2018 ). As gastric mucosal lesion is the main pathophysiological link of gastric ulcers, gastritis, and many other gastric diseases, it is also considered by World Health Organization (WHO) as the inevitable mode of inducing gastric ulcers, chronic gastritis, atrophic gastritis, intestinal metaplasia, atypical hyperplasia, and finally developing into gastric cancer (Da et al.…”