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. 2012 Oct 15;436(1-2):154-60.
doi: 10.1016/j.ijpharm.2012.05.063. Epub 2012 Jun 18.

Therapeutic effects of muscovite to non-steroidal anti-inflammatory drugs-induced small intestinal disease

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Therapeutic effects of muscovite to non-steroidal anti-inflammatory drugs-induced small intestinal disease

Guanqun Chao et al. Int J Pharm. .

Abstract

Objective/background: The ability of non-steroidal anti-inflammatory drugs (NSAIDs) to injure the small intestine has been well established in humans and animals. Muscovite is one kind of natural clay consisting of an insoluble double silicate of aluminum and magnesium. It has been developed and marketed in China for the treatment of gastric diseases. The present study was designed to examine the effects of intragastric treatment of muscovite on the intestinal damage induced by administration of diclofenac in rat.

Methods: Male SD rats were treated with muscovite for 9 days, with concomitant treatment with anti-inflammatory doses of diclofenac on the final 5 days. The anatomical lesion, villous height, the thickness and the section area of small intestine were quantitatively analyzed. The change of ultrastructural organization was observed. Endotoxin level in blood was measured by photometry. Epidermal growth factor was observed by immunohistochemistry.

Results: Muscovite decreased the macroscopic and histologic damage induced by diclofenac in the rat small intestine. In the muscovite group, villous height (139.8±13.2 μm) was higher than which of the model group (86.6±17.1 μm) (P<0.05). The index of the thickness and the section area was higher than model group. LPS level in the portal blood of muscovite (0.84±1.17 EU/ml) was lower than model group (4.52±0.98 EU/ml) (P<0.05). The EFG of muscovite group was higher significantly compared with the model group (P<0.05).

Conclusion: Muscovite can protect the small intestine from the damage induced by diclofenac in the conscious rat. Muscovite can repair NSAID-induced intestinal damage at least in part because of significant lesion in mechanical barrier function and reduction in epidermal growth factor.

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