马黛通络饮对小鼠动脉粥样硬化血管内皮损伤的保护作用
2017,49(10):1-4
摘要:目的:研究马黛通络饮对动脉粥样硬化(AS)小鼠模型血管内皮损伤的保护作用机制。方法:选取5周龄雄性AopE-/-鼠48只,随机分为模型组、辛伐他汀组和马黛通络饮高、低剂量组,相同遗传背景C57BL/6J雄性小鼠为正常对照组,共5组,每组12只。除正常对照组外,其余各组给予高脂饲料喂养4周造模,马黛通络饮高、低剂量组每天给予马黛通络饮煎剂20 g/(kg·d)、10 g/(kg·d)灌胃,辛伐他汀组每天给予辛伐他汀稀释液0.01 g/(kg·d)灌胃,正常对照组和模型组灌胃等体积的生理盐水。连续灌胃8周后,采用ELISA法检测各组小鼠主动脉组织中的肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、单核细胞趋化蛋白1(MCP-1)、内皮源型一氧化氮合酶(eNOS)水平,Western blot法检测核转录因子-κB(NF-κB)的水平。结果:与正常对照组比较,模型组、辛伐他汀组、马黛通络饮低剂量组、马黛通络饮高剂量组小鼠主动脉组织中的TNF-α、IL-6、ICAM-1、VCAM-1、MCP-1、NF-κB水平显著升高,eNOS显著降低,差异均有统计学意义(P<0.05,P<0.01)。与模型组比较,辛伐他汀组、马黛通络饮低剂量组、马黛通络饮高剂量组小鼠主动脉组织中的TNF-α、IL-6、ICAM-1、VCAM-1、MCP-1、NF-κB显著降低,eNOS显著升高,差异均有统计学意义(P<0.05,P<0.01)。结论:马黛通络饮通过抑制NF-κB信号通路的活性,降低Apo E基因敲除小鼠主动脉内TNF-α、IL-6、ICAM-1、VCAM-1、MCP-1等炎性因子、黏附分子、趋化因子水平,增加了eNOS的表达,达到抑制炎症浸润、保护血管内皮的作用。
关键词:马黛通络饮; 动脉粥样硬化; 炎性因子; 黏附分子; 趋化因子; 动物实验; 小鼠;
Abstract:Abstract:Objective:To study the protective effect of Madai Tongluo yin on vascular endothelial injury of atherosclerosis(AS)model mice.Methods:Selected 48 male AopE-/-mice of 5-week old,and divided them into the model group,simvastatin group,high dose Madai Tongluo yin group and low dose Madai Tongluo yin group,and normal control group consisting of C57BL/6J mice with the same genetic background,12 cases in each.Except normal control group,the other groups were all given high-fat diet for modeling.The high dose and the low dose Madai Tongluo yin groups were given Madai Tongluo yin of 20 g/(kg·d)and 10 g/(kg·d)every day by gavage respectively,while the simvastatin group was given dilution of simvastatin of 0.01 g/(kg·d)by gavage,normal control group and the model group were given equal volume of normal saline.After constantly gavage for eight weeks,detected level of tumor necrosis factor-α(TNF-α),interleukin-6,intercellular adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1),monocyte chemoattractant protein-1(MCP-1),endothelial nitric oxide synthase(eNOS)with enzyme-linked immunosorbent assay(ELISA),and detected level of nuclear factor-KappaB(NF-κB)with Western blot.Results:Compared with normal control group,levels of TNF-α,IL-6,ICAM-1,VCAM-1,MCP-1 and NF-κB in aortic tissue of the model group,simvastatin group,high dose Madai Tongluo yin group and low dose Madai Tongluo yin group were significantly increased,while eNOS were significantly decreased,the differencebeing significant(P<0.05,P<0.01).Compared with the model group,levels of TNF-α,IL-6,ICAM-1,VCAM-1,MCP-1 and NF-κB in the aortic tissue of the simvastatin group,high dose Madai Tongluo yin group and low dose Madai Tongluo yin group were significantly decreased,while eNOS levels were significantly increased,the difference being significant(P<0.05,P<0.01).Conclusion:Madai Tongluo yin can reduce levels of TNF-α,IL-6,ICAM-1,VCAM-1,MCP-1 and NF-κB by inhibiting activity of NF-κB signal of AopE-/-mice.It increases the expression of eNOS and exerts actions of inhibiting inflammatory infiltration and protecting vascular endothelium.
Key words:Madai Tongluo yin;Atherosclerosis;Inflammatory factor;Adhesionmolecule;Chemokine;Animal experiment;Mice
收稿日期:
基金项目: