王不留行黄酮苷对小鼠动脉粥样硬化的作用及机制

Effect of Vaccarin on atherosclerosis in mouse model and its mechanism

目的探讨王不留行黄酮苷(vaccarin)在小鼠动脉粥样硬化模型中的作用及其分子机制。方法采用AopE^(-/-)小鼠构建动脉粥样硬化模型,其中药物干预组采用腹腔注射vaccarin。采用油红O染色测定主动脉及主动脉根部的脂质,ELISA法测定血清炎症因子等指标。结果王不留行黄酮苷给药组(ApoE^(-/-)+HFD+Vaccarin)与模型组结论vaccarin可抑制主动脉内皮动脉粥样硬化斑块的形成,降低小鼠动脉粥样硬化斑块的纤维化程度、炎症及凋亡水平,且vaccarin可通过影响ROS/p38 MAPK信号通路改善动脉粥样硬化。

Aim To investigate the effect of vaccarin on mouse atherosclerosis in vivo and the underlying mechanism.Methods AopE^(-/-)mice aged 6 to 8 weeks old were used to establish the atherosclerosis model.Oil red O staining was used to determine the lipid levels in aorta and aortic root.Enzyme linked immunosorbent assay(ELISA)was used to detect the levels of serum inflammatory factors.Results Vaccarin could effectively reduce the levels of blood glucose and blood pressure in AopE^(-/-)+HFD mice.Compared with AopE^(-/-)+HFD group,the fibrosis of vascular plaque in ApoE^(-/-)+HFD+Vaccarin group significantly decreased.The levels of TG,TC and LDL-C significantly decreased,while HDL-C increased by vaccarin intervention.Meanwhile,Vaccarin inhibited the serum levels of IL-6,MCP-1,ICAM-1 and VCAM-1 of AopE^(-/-)+HFD group.Finally,we found that vaccarin also inhibited the production of ROS and the phosphorylation of p38 MAPK protein in AopE^(-/-)+HFD group.Conclusion Vaccarin alleviates atherosclerosis by inhibiting ROS/p38 MAPK signaling pathway.