摘要
目的研究莪棱油自乳化剂对应激性胃黏膜损伤的保护作用及机制。方法采用水浸拘束法建立胃溃疡模型,以复方莪术油软胶囊为对照,评价胃黏膜损伤指数,分析血浆中超氧化物歧化酶(SOD)的活性、丙二醛(MDA)的含量,检测胃壁结合黏液量及胃组织前列腺素E2(PGE2)水平。结果与模型组比较,莪棱油自乳化剂高剂量组(260 mg·kg-1)小鼠应激性胃溃疡指数显著降低(P<0.01),其抗溃疡作用优于复方莪术油软胶囊(260 mg·kg-1)。莪棱油自乳化剂可显著降低胃黏膜损伤小鼠血浆中MDA含量,提高SOD活性及胃组织PGE2水平(P<0.01或P<0.05),且具有量效关系。结论莪棱油自乳化剂能有效抑制应激性胃溃疡的形成,其作用机制可能与提高氧自由基清除能力及促进胃黏膜防御因子PGE2的分泌有关。
Objective To investigate the protective effects of the eleng oil SEDDS on gastric ulcer induced by stress in mice and its mechanism. Methods The mice gastric ulcer model was induced by water immersion and immobilization. The control group was treated with compound zedoary turmeric oil soft capsule. The gastric mucosal ulcer index and the concentration of SOD, MDA in plasma were evaluated and measured. The amounts of PGE2 in stomach homogenate and gastfiLc wall mucus were also characterized. Results Com- pared with that of model group, the ulcer index of the treatment group significantly decreased in the high dose of eleng oil SEDDS (P 〈0. 01 ), and its anti-ulcer effects were better than those of compound zedoary turmeric oil soft capsule. Furthermore, the eleng oil SEDDS could significantly decrease the concentration of MDA,while the activities of SOD and the contents of PGE2 were obviously increased (P 〈0. 01 or P 〈 0. 05 ) in a dose-dependant manner. Conclusions The eleng oil SEDDS can effectively inhibit the formation of stress gastric ulcer. The mechanism may be related to enhancing the scavenging effects of oxygen free rad- ical and promoting the secretion of gastric mucosal defense factor, which is PGE2,in mice.
出处
《沈阳药科大学学报》
CAS
CSCD
北大核心
2014年第2期134-137,共4页
Journal of Shenyang Pharmaceutical University
基金
国家自然科学基金面上资助项目(30973949)
山东省自然科学基金资助项目(ZR2009CM)