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机构地区:[1]广州中医药大学脾胃研究所,广东省广州市510405 [2]河南中医学院,河南省郑州市450008
出 处:《世界华人消化杂志》2008年第29期3321-3323,共3页World Chinese Journal of Digestology
基 金:广州中医药大学创新基金资助项目;No.200607F31~~
摘 要:目的:探讨黄芪总苷对应激大鼠胃黏膜褪黑素受体基因表达及氧自由基变化的影响.方法:SD大鼠48只分为4组,即正常对照组,模型组,黄芪总苷组和雷尼替丁组,每组12只.采用水浸-束缚应激模型,观察胃黏膜损伤指数,比色法检测胃黏膜SOD活性、MDA含量,RT-PCR法测定褪黑素受体1、2亚型mRNA表达变化.结果:与正常组比较,模型组大鼠胃黏膜损伤指数明显增高,MDA含量增高,SOD活性下降,褪黑素受体1、2基因表达降低,黄芪总苷预防给药后可明显降低应激大鼠胃黏膜损伤指数(6.75±4.10vs16.83±4.96,P<0.01)和MDA含量(0.45±0.07vs0.79±0.36,P<0.05),升高SOD活性(110.62±26.42vs71.74±22.20,P<0.05)和褪黑素受体1、2基因表达(0.86±0.12vs0.54±0.05,0.79±0.14vs0.50±0.10,均P<0.01).结论:黄芪总苷对水浸-束缚应激大鼠胃黏膜损伤有保护作用,其保护机制可能与调节胃黏膜褪黑素受体,并参与抗氧自由基损伤有关.AIM: To investigate the effects of astragaloside (AST) on gene expression of melatonin receptor and oxygen free radical in gastric mucosa of rat with stress ulcer. METHODS: A total of 48 experimental animals were equally divided into 4 groups: the control group, the model group, the AST group and the ranitidine group. The stress ulcer model was established using water immersion and restraint. The SOD activity, the MDA contents were determined using colorimetry, and the expression of melatonin receptors 1 and 2 were detected in gastric mucosa using RT-PCR. RESULTS: Compared with the control group, the model group showed increased ulcer index and elevated MDA contents, decreased SOD activity and down-regulated mRNA expression of melatonin receptors in damaged gastric mucosa. After administration of AST, the gastric mucosal ulcer index decreased significantly (6.75 ± 4.10 vs 16.83 ± 4.96, P 〈 0.01) and MDA contents were relieved obviously (0.45 ± 0.07 vs 0.79 ± 0.36, P 〈 0.05). The SOD activity (110.62 ± 26.42 vs 71.74± 22.20, P 〈 0.05) and the expression of melatonin receptor1, 2 mRNA were significantly elevated (0.86± 0.12 vs 0.54 ± 0.05, 0.79 ± 0.14 vs 0.50 ± 0.10, both P 〈 0.01). CONCLUSION: AST could prevent the gastric mucosal damage of rats with stress ulcer. And the mechanism of the gastric mucosal protection is perhaps concerned with regulating melatonin receptor and lessening the injury of oxygen free radicals.
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