| 权媛,钱民章.绞股蓝总甙对高脂诱导动脉粥样硬化大鼠炎性分子表达的影响[J].,2010,30(4):403-406 |
| 绞股蓝总甙对高脂诱导动脉粥样硬化大鼠炎性分子表达的影响 |
| Effect and Mechanism of Gypenosides on the Inflammatory Molecular Expression in High-fat Induced Atherosclerosis Rats |
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| DOI： |
| 中文关键词: 病理生理学 动脉粥样硬化 绞股蓝总甙 氧化应激 炎症 |
| 英文关键词:pathophysiology atherosclerosis gypenosides oxidative stress inflammation |
| 基金项目:贵州省科技厅资助项目(No.黔科合J字[2009]2178号) |
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| 中文摘要: |
| 目的研究绞股蓝总甙(gyrenosides,GP)对高脂诱导动脉粥样硬化(AS)大鼠病变部位炎性因子表达的影响及可能机制。方法采用高脂饲料喂饲和腹腔注射维生素D3建立大鼠AS模型。60只雄性健康SD大鼠随机分为正常组、模型组、GP 3个剂量组、辛伐他汀组。7周后处死大鼠,光镜下观察胸主动脉病理学改变;免疫组织化学染色法检测主动脉壁细胞间黏附分子-1(ICAM-1)、单核细胞趋化蛋白-1(MCP-1)和核因子κB p65(NF-κB p65)的表达;ELISA法测定血清氧化型低密度脂蛋白水平(ox-LDL);比色法测定血清总抗氧化能力、硫代巴比妥酸法测定血清丙二醛(MDA)水平。结果与模型组比较,GP各剂量组可减轻AS病变;下调主动脉壁ICAM-1、MCP-1和NF-κBp65的表达(P<0.01);降低血清MDA、ox-LDL水平(P<0.01),升高血清总抗氧化水平(P<0.01)。结论GP可下调ICAM-1及MCP-1的表达、抑制实验性大鼠AS病变的形成,其机制可能与其抗氧化进而抑制NF-κB的激活有关。 |
| 英文摘要: |
| Objective To evaluate the effect and possible mechanism of gypenoside(GP) on expression of inflammatory factors in aortic lesion of rats with high-fat induced atherosclerosis.Methods Atherosclerotic rat model was established by feeding high-fat diet and intraperitoneal injection of vitamin D3.Sixty healthy male SD rats were randomly divided into the normal group,the model group,the simvastatin treated group and the three GP groups treated respectively with different dosages of GP.Rats were sacrificed 7 weeks later,their histopathological changes in thoracic aorta were observed by light microscope;expressions of intercellular adhesion molecule 1(ICAM-1),monocyte chemotactic protein-1(MCP-1) and nuclear factor-κBp65(NF-κBp65) in aortic wall were detected by immunohistochemistry;serum level of oxidized low-density lipoprotein(ox-LDL) was determined by ELISA;serum total antioxidant capacity determined by colorimetry,and serum malondialdehyde(MDA) level determined by Thiobarbituric acid method.Results In comparing with the model group,GPS showed actions in lessening the atherosclerosis lesion;reducing expressions of ICAM-1,MCP-1 and NF-κBp65 in aortic wall(P<0.01) and serum levels of MDA,ox-LDL(P<0.01),as well as increasing the serum level of total antioxidant capacity(P<0.01).Conclusion GP can down-regulate the expressions of ICAM-1 and MCP-1,inhibit the atherosclerosis formation in experimental rats,its mechanism might be related with its anti-oxidation effect and further inhibiting on the NF-κB activation. |
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