基于内皮功能改善的针刺抗胰岛素抵抗分子机制研究

This research is established on the foundation of previous studies. In this research, the subjects are the model rats with spontaneous insulin resistance (Otsuka Long-Evans Tokushima Fatty rats, OLETF rats). Aiming at the endothelial dysfunction during the progression of insulin resistance, to observe acupuncture's improving effects on this dysfunction, to explore the cellular mechanism through observing the endothelial cells apoptosis and its modulating genes-bax/bcl-2, to explore the molecular mechanism through observing the PI3K-NO and MAPK-ET1 signal pathways which are mayor pathways modulating vasodilator and vasoconstriction. In this research, we advance the hypothesis that improving endothelial dysfunction is one of the effecting pathways for acupuncture reversing insulin resistance, the key molecular mechanism is the balance between PI3K-NO signal pathway and MAPK-ET1 signal pathways. This hypothesis would be verified by rigorous experimental design and advanced experimental technology. The conclusions of this research would supply scientific evidence for acupuncture reversing insulin resistance and preventing atherosclerosis and supply steady theory for acupuncture treatment on artery diseases related to insulin resistance, such as cerebral infarction and coronary disease in clinic.

本课题在既往研究基础上，以自发性胰岛素抵抗模型大鼠（Otsuka Long-Evans Tokushima Fatty rats，OLETF大鼠）为研究对象，针对胰岛素抵抗过程中所产生的血管内皮功能障碍，观察针刺改善胰岛素抵抗内皮功能紊乱的效应，并通过观察动脉血管内皮细胞凋亡及其调控基因bax/bcl-2探讨其细胞机制，通过观察动脉内皮PI3K-NO和MAPK-ET1两条调节血管舒缩功能的信号通路探讨其分子机制。本课题提出"针刺改善血管内皮功能障碍是针刺抗胰岛素抵抗的作用途径之一，而PI3K-NO信号通路和MAPK-ET1信号通路的平衡是其发挥作用的关键分子机制"的假说，其研究结果将为针刺干预胰岛素抵抗、预防动脉粥样硬化提供强有力的科学证据，并为临床应用针灸治疗脑梗塞、冠心病等胰岛素抵抗相关血管疾病奠定坚实的理论基础。

以自发性胰岛素抵抗模型大鼠（Otsuka Long-Evans Tokushima Fatty rats, OLETF大鼠）为研究对象，观察到针刺改善了胰岛素抵抗内皮功能紊乱的效应。本课题验证了“针刺改善血管内皮功能障碍是针刺抗胰岛素抵抗的作用途径之一，而PI3K-NO信号通路和MAPK-ET1信号通路的平衡时其发挥作用的关键分子机制”的假说，其研究成果将为针刺干预胰岛素抵抗、预防动脉粥样硬化提供强有力的科学证据，并为临床应用针灸治疗脑梗塞、冠心病等胰岛素抵抗相关血管疾病奠定坚实的理论基础。