摘要
目的:研究岩藻多糖对急性酒精性损伤模型大鼠胃黏膜的保护作用,为胃黏膜保护类功能食品开发提供科学依据。方法:将60只SD大鼠随机分成空白对照组、模型组、海藻多糖各剂量组【0.083,0.167,0.334 g/(kg BW)】、阳性对照组【(甲氰咪胍,0.8 g/(kg BW)】,每组各10只。采用酒精灌胃致胃黏膜损伤模型。给予岩藻多糖30d后,观察胃黏膜组织的大体和病理组织改变,测定胃组织前列腺素E2含量、丙二醛含量、NO含量及超氧化歧化酶活力。结果:岩藻多糖能明显改善胃黏膜组织损伤情况,降低损伤积分(P<0.05),提高酒精性损伤抑制率;在高剂量组能提高大鼠胃组织氧化歧化酶活力(P<0.05);各剂量组均能提高大鼠胃组织前列腺素E2含量(P<0.01)和NO含量(P<0.05),降低大鼠胃组织丙二醛含量(P<0.05)。结论 :岩藻多糖对大鼠急性酒精性胃粘膜损伤具有一定保护作用,其机制可能与增强胃黏膜保护因子,提高抗氧化和降低脂质过氧化能力有关。
Objective: The protective effects and mechanism of Fucoidin on the ethanol-induced gastric mucosal lesion of rats in vivo were investigated to supply scientific base for functional development of Fucoidin. Methods : 60 SD rats were randomly divided into fucoidin groups(0.083, 0.167, 0.334 g/(kg BW)), negative control group, model group,and positive control group(colloidal Cimetidine,0.8 g/(kg BW)). There were 10 cases in each group. The model of acute gastric mucosa injure was induced with 95% acetic acid. After treated with fucoidin for 30 days, the general and pathological integral of gastric mucosa lesion were observed. The levels of PGE2、NO、SOD、MDA were measured as per instructions of assay kits. Results: Fucoidin could significantly reduce the lesion of gastric mucosal by decreasing damage ingegral(P〈0.05)and increasing the inhibitory rate of fucoidin on ethanol-induced damage. All dose of fucoidins could raise the levels of PGE2 and NO and decease the levels of MDA induced by ethanol in gastric mucosa tissues of rats.The SOD activity were reduced only in 0.334 g/(kg BW) group of fucoidin. Conclusion: Fucoidin shows a protective effect on ethanol-induced gastric mucosal lesion in rats and its mechanism may be related to the increase of protective factor, anti-oxidative capacity and the decrease of lipid peroxidation in rats
出处
《中国食品学报》
EI
CAS
CSCD
北大核心
2015年第1期19-24,共6页
Journal of Chinese Institute Of Food Science and Technology