Department of Family Medicine, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou Qingchun Road No. 3, 310016, China.
Int J Pharm. 2012 Oct 15;436(1-2):154-60. doi: 10.1016/j.ijpharm.2012.05.063. Epub 2012 Jun 18.
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.
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.
目的/背景：非甾体抗炎药（NSAIDs）损伤小肠的能力在人类和动物中已得到充分证实。软锰矿是一种由不溶性铝镁双硅酸盐组成的天然粘土。它已在中国开发并用于治疗胃病。本研究旨在研究软锰矿灌胃给药对双氯芬酸诱导大鼠肠道损伤的影响。
雄性 SD 大鼠用软锰矿治疗 9 天，同时在最后 5 天给予抗炎剂量的双氯芬酸。定量分析解剖损伤、绒毛高度、小肠厚度和截面积。观察超微结构组织的变化。用比色法测定血液内毒素水平。用免疫组化法观察表皮生长因子。
软锰矿降低了双氯芬酸诱导的大鼠小肠的大体和组织学损伤。在软锰矿组，绒毛高度（139.8±13.2μm）高于模型组（86.6±17.1μm）（P<0.05）。厚度和截面积指数高于模型组。软锰矿门静脉血液中的 LPS 水平（0.84±1.17 EU/ml）低于模型组（4.52±0.98 EU/ml）（P<0.05）。软锰矿组的 EFG 明显高于模型组（P<0.05）。
软锰矿可保护清醒大鼠免受双氯芬酸引起的小肠损伤。软锰矿可修复 NSAID 诱导的肠道损伤，至少部分原因是机械屏障功能明显受损和表皮生长因子减少。
