检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:祝晓庆[1] 杨洁[1] 邵娟[1] 刘超[1] 吴基良[1]
机构地区:[1]湖北科技学院糖尿病心脑血管病变湖北省重点实验室,湖北咸宁437100
出 处:《中国药理学通报》2017年第2期180-184,共5页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No81270355)
摘 要:目的探讨复方总黄酮对ApoE基因敲除小鼠动脉粥样硬化的保护作用。方法 15只7周龄的♂C57BL/6小鼠普通饮食为正常对照组;75只7周龄的♂ApoE基因敲除小鼠高脂饮食,随机分为5组:模型组、辛伐他汀组、低剂量复方总黄酮组、中剂量复方总黄酮组、大剂量复方总黄酮组。灌胃16周造模完成后,采集血清,分离胸主动脉。HE染色检查胸主动脉斑块,检测血脂4项(TC、TG、LDL-C、HDL-C)和血清SOD;ELISA检测IL-1β、NF-κB值。结果模型组胸主动脉斑块明显,复方总黄酮组斑块均不同程度变小。复方总黄酮组的TC、TG、LDL-C、IL-1β、NF-κB明显降低,HDL-C、SOD含量明显升高,与模型组比较差异有显著性(P<0.05)。结论复方总黄酮对小鼠早期动脉粥样硬化有良好的保护作用,可能与其降脂抗炎作用有关。Aim To investigate the protective effect of compound total flavonoids on atherosclerosis in ApoE^-/- knockout mice.Methods Seven-week old C57BL/6 mice considered of the normal group (n =1 5 );seven-week old ApoE^-/- mice were fed with high-fat diet and were assigned randomly into 5 groups:model group,simvastatin group,the low com-pound flavonoids group,the middle compound fla-vonoids group and the high compound flavonoids group.After 1 6 weeks,mice serum and aortas were harvested.The formation of atherosclerotic plaque was analyzed by HE staining,The serum level of lipids pro-files and superoxide dismutase (SOD )were deter-rnined.The levels of IL-1 βand NF-κB in serum were detected by ELISA assay.Results Area of atheroscle-rotic lesion was significantly less in the compound fla-vones group than in model.The level of TC,TG,LDL-C,IL-1 β,NF-κB in serum of the compound flavonoids group were decreased significantly,while SOD and HDL-C increased significantly compared with the mod-el group,and the difference was significant (P 〈0.05).Conclusion The compound flavonoids have a good protective effect on early atherosclerosis in mice, which may be due to its alleviating effects on hyperlipi-demia and inflammation and oxidation.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.69