苍术素对脾虚证大鼠胃黏膜超微结构及胃肠功能的影响

Effects of atractylodin on ultrastructure of gastric mucosa and gastrointestinal function of rats with syndrome of spleen deficiency

目的:观察苍术素对实验性脾虚湿阻证大鼠胃黏膜保护及胃肠功能障碍的影响,阐明其作用机制。方法:采用小承气汤煎剂加饥饱失常建立脾虚证大鼠模型,共造模15d,造模结束后,苍术素组苍术素溶液灌服,正常组和模型组则双蒸水对照灌胃,持续10d。炭末灌胃法行大鼠胃内残留率、小肠推进比的测定,HE染色行大鼠胃黏膜病理学观察,透射电镜法观察腺胃区胃黏膜组织细胞及细胞间连接的超微结构改变,免疫组化法测定大鼠胃黏膜组织中三叶因子1(TFF1)及结肠组织中c-kit的表达量。结果:病理观察显示,苍术素可明显改善脾虚湿阻证大鼠胃黏膜形态学及胃黏膜细胞的超微结构异常,与模型组比较,苍术素高、中、低剂量组的胃内残留率明显下降、小肠推进比明显升高(P<0.05,P<0.01);胃黏膜组织中TFF1和结肠组织中c-kit的表达量亦不同程度升高(P<0.05,P<0.01)。结论:苍术素可整体改善由于脾虚而导致的大鼠胃黏膜损害,并可调治因脾虚而导致的胃肠功能紊乱。

Objective： To observe the protective effect of atractylodin on gastric mucosa and its influence on gastrointestinal function of rats with syndrome of spleen deficiency, in order to clarify its action mechanism. Methods： The rat models with syndrome of spleen deficiency were established by using Xiaochengqi Decoction combined with irregular eating, and the modeling time lasted for 15 days. After modeling, the rats in atractylodin groups received gavage administration with atractylodin solution, and rats in control and model groups received gavage administration with double distilled water for 10 days. The gastric remnant rate and small intestinal transit ratio were detected by using gavage administration with charcoal powder. The gastric mucosa pathological variation was observed by using HE staining method. The changes in ultrastructure in cells and intercellular junction of gastric mucosa in gland region were observed by using transmission electron microscopy. The expression of TFF1 in gastric mucosa and c-kit in colon tissue was tested by using immunohistochemistry. Results： Pathological observation showed that atractylodin could improve the abnormal ultrastructure in gastric mucosal cells of rats with syndrome of dampness stagnancy due to spleen deficiency. Compared with model group, the gastric remnant rate of rats in high, middle and low dosage of atractylodin groups was declined obviously, and the small intestinal transit ratio of rats in these groups was increased obviously（P0.05, P0.01）. The expression of TFF1 in gastric mucosa and c-kit in colon tissue was increased on different levels（P0.05, P0.01）. Conclusion： Atractylodin could exert the overall improvement in rat gastric mucosal damage due to spleen deficiency, and regulate and treat the functional gastrointestinal disorders due to spleen deficiency.