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作 者:曾平[1] 符秀琼[2] 王启瑞[2] 范钦[2] 贾钰华[2] 孙学刚[2]
机构地区:[1]广东省人民医院 [2]南方医科大学中医药学院分子生物学实验室,广州510515
出 处:《中药药理与临床》2009年第6期11-13,共3页Pharmacology and Clinics of Chinese Materia Medica
基 金:国家自然科学基金(30572435);广东省自然科学基金(06024430);广东省自然科学基金博士启动基金(05300461)
摘 要:目的:研究加味补阳还五汤对动脉粥样硬化斑块形成及炎症细胞因子表达谱的影响及其转录调控机制。方法:应用apoE-/-小鼠制作动脉粥样硬化模型,病理切片观察动脉粥样硬化形成情况,常规方法检测总胆固醇(TC)、甘油三酯(TG)和高密度脂蛋白胆固醇(HDL),应用LiquiChip检测细胞因子表达谱,凝胶迁移率变动分析观察NF-κB活化水平。结果:加味补阳还五汤显著减轻动脉粥样形成,显著减少斑块面积;降低TG和TC,升高HDL;降低肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)和IL-18水平,降低NF-κB的活化(P<0.05)。结论:加味补阳还五汤能显著改善apoE-/-小鼠动脉粥样硬化水平,与其降低TC、TG和升高HDL有关,加味补阳还五汤降低apoE-/-小鼠炎症因子水平,可能与其降低NF-κB的活化有关。Objective :To investigate the effects of Modified Buyanghuanwu Recipe on the formation of atherosclerotic plaque and cytokine profiles and its transcriptional mechanism. Methods: Apelipoprotein E knockout mice (apoE/) were used to replicate atherosclerosis model and slices of aorta were stained with hematoxylin and eosin (HE) and area of plaques were analyzed. Total cholesterol (TC), triglycerides (TG) and high density lipoprotein (HDL) were measured by routine methods. Cytokine profiles were obtained through liquichip. Electrophoretie mobility shift assay (EMSA) was used to analyze the activation of nuclear factor kappa B (NF-KB). Results: Modified Buyanghuanwu Recipe alleviated the formation of atherosclerosis that the area of plaques were reduced significandy compared with model group ( P 〈 0.05). TG (P〈0.01) and TC (P〈0.01) were reduced and HDL (P 〈0.01) was elevated in Modified buyanghuanwu Recipe group compared with model group. Furthermore, tumor necrosis factor α (TNF-α) (P 〈0.01 ), interleukin 6 (IL-6) (P 〈0.01 ) and IL-18 (P 〈0.05) were reduced and activation of NF-κB (P 〈 0.05) was decreased by Modified Buyanghuanwu Recipe compared to model group. Conclusions: The effects of Modified Buyanghuanwu Recipe in ameliorating the formation of atherosclerosis might have relationship with the decrease of TG and TC and increase of HDL. The downregulation of TNF-α, IL-6 and IL-18 of Modified Buyanghuanwu Recipe might regulated by lowered activation of NF-κB.
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