Quan Yuan, Qian Min-zhang
Department of Biochemistry, Zunyi Medical College, Guizhou.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2010 Apr;30(4):403-6.
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.
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-kappaBp65 (NF-kappaBp65) 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.
In comparing with the model group, GPS showed actions in lessening the atherosclerosis lesion; reducing expressions of ICAM-1, MCP-1 and NF-kappaBp65 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 ).
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-kappaB activation.
评价绞股蓝总苷（GP）对高脂诱导的动脉粥样硬化大鼠主动脉病变中炎症因子表达的影响及其可能机制。
通过高脂饮食喂养和腹腔注射维生素D3建立动脉粥样硬化大鼠模型。将60只健康雄性SD大鼠随机分为正常组、模型组、辛伐他汀治疗组和3个不同剂量GP治疗组。7周后处死大鼠，光镜观察胸主动脉组织病理学变化；免疫组化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；酶联免疫吸附测定法（ELISA）检测血清氧化型低密度脂蛋白（ox-LDL）水平；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。
与模型组比较，GP能减轻动脉粥样硬化病变；降低主动脉壁ICAM-1、MCP-1和NF-κB p65的表达（P<0.01）以及血清MDA、ox-LDL水平（P<0.01），并提高血清总抗氧化能力水平（P<0.01）。
GP可下调ICAM-1和MCP-1的表达，抑制实验大鼠动脉粥样硬化形成，其机制可能与其抗氧化作用及进一步抑制NF-κB激活有关。
