Li-Na Meng1, Li Fang, Bin Lu. 1. Department of Gastroenterology, First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou. mln6713@163.com
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
OBJECTIVE: 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. METHODS: 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. RESULTS: 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). CONCLUSION: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.