PDF(Pubmed)
Abstract：
The malfunction of endothelial progenitor cells (EPCs) due to ox-LDL is a risk contributor for arteriosclerotic disease. Meanwhile, lycopene possesses anti-inflammatory and antioxidative qualities. This investigation aimed to determine if lycopene can protect EPCs from ox-LDL-induced damage and to elucidate the underlying mechanism. The effects of lycopene on the survival, migration, and tube-forming capacity of EPCs were determined via in vitro assays. Expression of proteins related to pyroptosis and cellular proteins related to AMPK/mTOR/NLRP3 signaling was determined by western blot/flow cytometry. Our results demonstrated that lycopene treatment significantly enhanced proliferation, tube formation, and migration of EPCs stimulated by ox-LDL. Additionally, lycopene was found to suppress pyroptosis in ox-LDL-induced EPCs through the activation of AMPK, which led to the inhibition of mTOR phosphorylation and subsequent downregulation of the downstream NLRP3 inflammasome. In summary, our study suggests that lycopene mitigates ox-LDL-induced dysfunction in EPCs and inhibits pyroptosis via AMPK/mTOR/NLRP3 signaling. Our study suggests that lycopene may act as promising therapies for preventing atherosclerosis.
摘要：
由于ox-LDL引起的内皮祖细胞（EPCs）功能障碍是动脉硬化疾病的风险因素。同时,番茄红素具有抗炎和抗氧化特性。这项研究旨在确定番茄红素是否可以保护EPCs免受ox-LDL诱导的损伤，并阐明其潜在机制。番茄红素对生存的影响，迁移,通过体外试验确定EPC的成管能力。通过蛋白质印迹/流式细胞术确定与焦亡相关的蛋白和与AMPK/mTOR/NLRP3信号传导相关的细胞蛋白的表达。我们的结果表明，番茄红素治疗显着增强增殖，管形成,ox-LDL刺激EPCs的迁移。此外,发现番茄红素通过激活AMPK抑制ox-LDL诱导的EPCs的焦亡，这导致mTOR磷酸化的抑制和随后下游NLRP3炎性体的下调。总之,我们的研究表明,番茄红素通过AMPK/mTOR/NLRP3信号传导减轻ox-LDL诱导的EPCs功能障碍,并抑制焦亡.我们的研究表明，番茄红素可能是预防动脉粥样硬化的有希望的疗法。
