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目的桃叶珊瑚苷(aucubin,AU)是杜仲、车前草、地黄等中草药的有效成分之一。现代药理学研究发现,AU对免疫、心脑血管、神经系统均有保护作用,但其作用机制尚不清楚。课题组前期研究证实AU可激活雌激素受体,提示AU可能通过雌激素信号通路发挥心血管保护作用。近年来越来越多的证据表明,心脏祖细胞(cardiac progenitor cells,CPCs)在心肌缺血组织损伤修复中发挥重要作用。方法为了进一步阐明AU的作用机制,该研究以小鼠CPCs为细胞模型,采用Incu Cyte活细胞成像、TUNEL、Western blot、定量PCR等方法探讨了AU对肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)诱导的CPCs凋亡的影响及其作用机制。结果AU可以降低由TNF-α诱导的CPCs凋亡,降低caspase-3蛋白质表达,上调Bcl-2/Bax水平,雌激素受体β(estrogen receptorβ,ERβ)抑制剂可阻断AU的抗凋亡作用,同时AU可使ERβ表达升高。结论 AU可以抑制由TNF-α诱导的CPCs凋亡,其部分作用机制为ERβ通路的激活。
Purpose Aucubin (AU) is one of the active ingredients of Chinese herbal medicines such as Eucommia, Plantain, Rehmannia. Modern pharmacological studies have found that AU on the immune, cardiovascular and cerebrovascular, the nervous system has a protective effect, but its mechanism of action is not yet clear. Our previous study confirmed that AU can activate the estrogen receptor, suggesting that AU may play a cardiovascular protective role through the estrogen signaling pathway. In recent years, more and more evidence shows that cardiac progenitor cells (CPCs) play an important role in the repair of myocardial ischemic injury. Methods In order to further elucidate the mechanism of action of AU, we used mouse CPCs as a cell model to investigate the effects of AU on tumor necrosis factor-α (TNF-α) expression using live cell imaging with Incu Cyte, TUNEL, Western blot and quantitative PCR , TNF-α) induced apoptosis of CPCs and its mechanism of action. Results AU could reduce the apoptosis of CPCs induced by TNF-α, decrease the expression of caspase-3 protein and up-regulate the level of Bcl-2 / Bax. Inhibitors of estrogen receptor β (ERβ) Role, AU can make ERβ expression increased. Conclusion AU can inhibit the apoptosis of CPCs induced by TNF-α, and part of the mechanism is the activation of ERβ pathway.