mica and Intestinal-Diseases

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.. 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.. 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).. 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.

Topics: Aluminum Silicates; Animals; Anti-Inflammatory Agents, Non-Steroidal; Diclofenac; Intestinal Diseases; Intestine, Small; Lipopolysaccharides; Male; Microscopy, Electron, Transmission; Protective Agents; Rats; Rats, Sprague-Dawley

To examine the efficacy of muscovite on non-steroidal anti-inflammatory drug (NSAID) associated intestinal injury in rats, and its influences on the expressions of inflammatory factors, tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappaB (NF-kappaB), for researching its possible mechanism of intestinal mucosal protection.. NSAID associated intestinal injury in rat was induced by intra-gastric infusion of diclofenac. Twenty-four male Sprague-Dawley rats were randomly and equally assigned to three groups: normal control group, model control group and Muscovite group, 8 in each group. The normal control group received physiological saline 1 mL/100 g and the other two groups received diclofenac 7.8 mg/kg respectively every day for 5 days; while to the Muscovite group, Muscovite 120 mg/kg was gastric infused once on the day before modeling, followed with 120 mg/kg per day, given an hour before diclofenac infusion in the modeling days. All rats were killed on the 6th day, their gross changes and histological injury of intestinal mucosa were observed and scored, serum level of TNF-alpha was assayed in radioimmunoassay and NF-kappaB activity was determined by immunohistochemistry.. The small dosage diclofenac administration can cause intestinal damage, revealing obviously erythema, erosion, multiple ulcer, intestinal stricture, even perforation, etc. Intestinal injury in the Muscovite group was obviously milder than that in the model control group, only showed changes of local congestion, edema and erosion. The scores of gross and histological intestinal features in the model control group were 4.38 +/- 1.41 and 4.00 +/- 1.85, while in the Muscovite group were 1.25 +/- 1.58 and 1.75 +/- 0.71, respectively, all higher than those in the normal control group (0.00 +/- 0.00 and 0.00 +/- 0.00, P < 0.01 and P < 0.05), respectively, but the elevation in the model control group were more significant (P < 0.05). Similar results were shown in comparisons of TNF-alpha and NF-kappaB levels between groups, the values were 6.19 +/- 2.76 and 1.38 +/- 1.19 in normal control; 22.20 +/- 5.42 and 5.75 +/- 0.46 in model control; 9.61 +/- 4.02 and 0.13 +/- 0.35 in the Muscovite group, respectively (all P < 0.01).. Muscovite could effectively reduce the NSAID associated intestinal mucosal injury by inhibiting the activity of NF-kappaB in intestinal mucosa, and down-regulating the expression of TNF-alpha in blood plasma, so muscovite is proved to have protective function for intestine.

Topics: Aluminum Silicates; Animals; Anti-Inflammatory Agents, Non-Steroidal; Intestinal Diseases; Intestinal Mucosa; Intestine, Small; Male; NF-kappa B; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha