甘草总黄酮抑制慢性萎缩性胃炎大鼠胃黏膜腺体萎缩及机制研究

Licoflavone suppresses gland atrophy of gastric mucosa and its mechanism in rats with chronic atrophic gastritis

目的探讨甘草总黄酮抑制慢性萎缩性胃炎(CAG)大鼠胃黏膜腺体萎缩及相关作用机制,评价萎缩性胃炎的治疗作用。方法采用去氧胆酸钠溶液自由饮用,同时配合酒精灌服刺激的多因素方法诱导CAG大鼠模型,模型复制成功后将动物随机分为模型对照组、维酶素对照组、甘草总黄酮高、低剂量组,药物组分别连续灌胃给药30 d后,HE染色观察胃组织病理学变化;测定大鼠胃液分泌量、ELISA检测胃蛋白酶活性及血清中GAS、IL-1β、IL-6水平。结果与正常对照组比较,模型对照组大鼠胃黏膜萎缩率、胃组织病理评分明显改变,胃液分泌量、胃蛋白酶活性、血清胃泌素含量明显下降(P<0.01);血清IL-1β、IL-6水平明显升高(P<0.01);与模型对照组比较,甘草总黄酮给药30 d后,甘草总黄酮高、低剂量组大鼠胃液分泌量、胃蛋白酶活性以及血清GAS明显升高(P<0.05);胃黏膜萎缩率、胃组织病理评分、血清IL-1β、IL-6水平明显降低(P<0.05)。结论甘草总黄酮能够有效抑制慢性萎缩性胃炎大鼠胃黏膜损伤,促进胃分泌功能,提高胃泌素水平及胃蛋白酶活性以增强胃黏膜的防御功能,同时抑制炎症因子的释放,减少黏膜炎症发生。

Aim To investigate the mechanism of li- coflavone on gland atrophy of gastric mucosa in rats and estimate its treatment in chronic atrophic gastritis （CAG）. Methods CAG model was induced in the SD rats by drinking of sodium deoxyeholate combined alco- hols for 100 days. CAG rats were divided randomly in- to the CAG control group, vitacoenzyme group, lieofla- vone high dose, low dose and normal control group. After 30 days of treatment by feeding licoflavone, gas- tric histopathologieal changes were observed by HE staining; volume of secrete gastric juice was tested; pepsin activity and serum gastrin （GAS）, interleukin- 1β （ IL-1β）, interleukin-6 （IL-6） level was determined by ELISA. Results The mucosa atrophy rate in CAG rats was significantly increased compared with that in normal control group. The histophathologieal score was significantly higher, and gastric juice secretion, pepsinactivity and serum GAS were significantly decreased （P 〈 0.01 ）, while IL-115, IL-6 level in serum in- creased significantly （P 〈 0. 01 ）. The gastric juice se- cretion, pepsin activity and serum GAS were signifi- cantly increased in licoflavone treatment groups （P 〈 0. 05）, while mucosa atrophy rate, histophathological score and serum IL-1β, IL-6 level were significantly decreased （ P 〈 0.05 ）. Conclusion Licoflavone can inhibit chronic atrophic gastritis and gastric mucosal in- jury, enhance the function of gastric secretion, increase the gastrin levels and the activity of pepsin to improve the gastric mucosal defensive function, and inhibit the release of proinflammatory factors.