Lab Anim Res.  2016 Mar;32(1):56-64. 10.5625/lar.2016.32.1.56.

Comparison of the response using ICR mice derived from three different sources to ethanol/hydrochloric acid-induced gastric injury

• Song SH
• Kim JE
• Go J
• Koh EK
• Sung JE
• Lee HA
• Choi KM
• Kim HD
• Jung YS
• Kim KS
• Hwang DY

• KMID: 2312154
• DOI: http://doi.org/10.5625/lar.2016.32.1.56

Abstract

Animal models for gastric ulcers produced by physical, pharmacological and surgical methods have been widely employed to evaluate therapeutic drugs and investigate the mechanism of action of this disease. ICR mice were selected to produce this model, even though several mice and rats have been widely used in studies of gastric ulcers. To compare the responses of ICR mice obtained from three different sources to gastric ulcer inducers, alterations in gastric injury, histopathological structure, and inflammation were measured in Korl:ICR (Korea NIFDS source), A:ICR (USA source) and B:ICR (Japan source) treated with three concentrations of ethanol (EtOH) (50, 70, and 90%) in 150 mM hydrochloric acid (HCl) solution. Firstly, the stomach lesion index gradually increased as the EtOH concentration increased in three ICR groups. Moreover, a significant increase in the level of mucosal injury, edema and the number of inflammatory cells was similarly detected in the EtOH/HCl treated group compared with the vehicle treated group in three ICR groups. Furthermore, the number of infiltrated mast cells and IL-1β expression were very similar in the ICR group derived from three different sources, although some differences in IL-1β expression were detected. Especially, the level of IL-1β mRNA in 50 and 90EtOH/HCl treated group was higher in Korl:ICR and A:ICR than B:ICR. Overall, the results of this study suggest that Korl:ICR, A:ICR and B:ICR derived from different sources have an overall similar response to gastric ulcer induced by EtOH/HCl administration, although there were some differences in the magnitude of their responses.

Keyword

Korl:ICR mice; Gastric ulcer; EtOH/HCl; Hemorrhagic lesions; Mast cells; IL-1β

MeSH Terms

Animals
Edema
Ethanol
Hydrochloric Acid
Inflammation
Mast Cells
Mice
Mice, Inbred ICR*
Models, Animal
Rats
RNA, Messenger
Stomach
Stomach Ulcer
Ethanol
Hydrochloric Acid
RNA, Messenger

Figure

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  Figure 1 Stomach lesions of the ICR mice administered ethanol (EtOH)/hydrochloric acid (HCl). (A) Morphological features were observed in the stomachs of ICR mice derived from three different sources after opening along the greater curvature. Arrows indicate the area of hemorrhagic lesions in the inner surface of the stomach. (B) After measurement of the area of visible erosive lesions, the lesion index was calculated using the formula described in the materials and methods. The data shown represent the means±standard deviation (SD) of three replicates.

• 

  Figure 2 Histopathological analysis of stomach tissue. After the collection of stomachs from the subset group, the histopathological changes in the slide sections of stomach tissue were identified by staining with hematoxylin and eosin followed by observation at 400× magnification. Abbreviations: L, lumen; GP, gastric pits; SC, surface mucous cells.

• 

  Figure 3 Analysis of mast cells. Infiltration of mast cells in the slide sections of stomach tissue was identified by staining with toluidine blue followed by observation at 400× magnification. Arrows indicate the infiltrated mast cells in the gastric pits of the stomach tissue. The data shown represent the means±standard deviation (SD) of three replicates.

• 

  Figure 4 Analysis of cytokine expression in stomach tissues. The levels of IL-1β in the stomach tissue of ICR mice from subset groups were detected by RT-PCR analysis using specific primers. The intensity of each band was determined using an imaging densitometer and the relative level of each protein was calculated based on the intensity of actin transcript as an endogenous control. The data shown represent the means±SD of three replicates. *P<0.05 relative to the Korl:ICR group.

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