Atherosclerosis (AS) is a chronic disease of the arterial wall where both innate and adaptive immunoinflammatory mechanisms are involved. Inflammation plays an important role in the pathological process of atherosclerosis at various stages. Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ, also known as WWTR1) behave as a novel drug target against atherosclerosis. Therefore, the mechanism relationship of YAP/TAZ, inflammation and AS was explored in this study. Experiments demonstrated that serine dephosphorylation and nuclear translocation of YAP was increased in ECs and pericytes induced by oxidative low-density lipoprotein (ox-LDL), while the inhibition of YAP degraded the expression of downstream inflammatory factors. The expression of YAP/TAZ and inflammation proteins (JNK, NF-κB and TNF-α) in ECs and pericytes was suppressed through the application of Sal-B. Besides, Sal-B protects ECs and pericytes from oxidative stress and apoptosis. In vivo, Sal-B reduced en face and aortic root sinus lesions size, and decreased the expression of inflammation related factors (IL-6, IL-1β, TNF-α) and ox-LDL in serum sample of ApoE^−/− mice fed a high fat diet. Therefore, our work provides a potential therapeutic strategy of using Sal-B to attenuate the development of atherosclerosis, the anti-atherosclerosis effects of Sal-B is related to regulate YAP/TAZ/JNK signaling pathway.

动脉粥样硬化（AS）是一种先天性和适应性免疫炎症机制都涉及的慢性动脉壁疾病。炎症在各个阶段的动脉粥样硬化的病理过程中起着重要作用。Yes相关蛋白（YAP）和具有PDZ结合基序的转录共激活因子（TAZ，也称为WWTR1）可以作为对抗动脉粥样硬化的新型药物靶标。因此，本研究探讨了YAP / TAZ，炎症和AS的机制关系。实验表明，氧化性低密度脂蛋白（ox-LDL）诱导的EC和周细胞中，YAP的丝氨酸去磷酸化和核易位增加，而对YAP的抑制则降低了下游炎症因子的表达。YAP / TAZ和炎症蛋白（JNK，通过使用Sal-B可抑制EC和周细胞中的NF-κB和TNF-α。此外，Sal-B保护EC和周细胞免受氧化应激和细胞凋亡。在体内，Sal-B可减少ApoE血清样品中面部和主动脉根窦病变的大小，并降低炎症相关因子（IL-6，IL-1β，TNF-α）和ox-LDL的表达^-/-小鼠喂养高脂饮食。因此，我们的工作提供了使用Sal-B减轻动脉粥样硬化发展的潜在治疗策略，Sal-B的抗动脉粥样硬化作用与调节YAP / TAZ / JNK信号通路有关。