Abstract：
OBJECTIVE: Endothelial cells (ECs) can provide cell protection for cardiomyocytes (CMs) under hypoxia-reoxygenation (HR) conditions by secreting derived factors. This study aimed to explore the role of curcumin (CUR) in ECs for protecting CMs from HR injury.
METHODS: A co-culture system for ECs and CMs was set up, and subjected to HR. The transcription, expression, and secretion of FGF2 were detected by RT-qPCR, western blot, and ELISA, respectively. siRNAs specifically targeting FGF2 were transfected into ECs. FGF2 receptor- specific inhibitors (AZD4547) were used to treat CMs.
RESULTS: The co-culture with ECs did not affect the proliferation of CMs, while CUR and ECs co-culture had a synergistic effect on promoting the proliferation of CMs in HR. Furthermore, the co-culture with ECs did not affect the apoptosis and autophagy of CMs in HR. However, the co-culture of ECs after CUR treatment inhibited the apoptosis and autophagy of CMs in HR. CUR treatment significantly enhanced FGF2 mRNA, protein, and secretion levels of ECs in HR. In addition, CUR treatment increased FGF2 levels in the CMs medium in the ECs and CMs co-culture system. The reduction of FGF2 levels in the medium and the inhibition of FGF2 receptors significantly inhibited the proliferation of CMs and significantly promoted the apoptosis and autophagy of CMs in HR.
CONCLUSIONS: Focusing on the protective effects of CUR and ECs on cardiomyocytes is of great significance for the treatment of clinical myocardial HR injury.
METHODS: A co-culture system for ECs and CMs was set up, and subjected to HR. The transcription, expression, and secretion of FGF2 were detected by RT-qPCR, western blot, and ELISA, respectively. siRNAs specifically targeting FGF2 were transfected into ECs. FGF2 receptor- specific inhibitors (AZD4547) were used to treat CMs.
RESULTS: The co-culture with ECs did not affect the proliferation of CMs, while CUR and ECs co-culture had a synergistic effect on promoting the proliferation of CMs in HR. Furthermore, the co-culture with ECs did not affect the apoptosis and autophagy of CMs in HR. However, the co-culture of ECs after CUR treatment inhibited the apoptosis and autophagy of CMs in HR. CUR treatment significantly enhanced FGF2 mRNA, protein, and secretion levels of ECs in HR. In addition, CUR treatment increased FGF2 levels in the CMs medium in the ECs and CMs co-culture system. The reduction of FGF2 levels in the medium and the inhibition of FGF2 receptors significantly inhibited the proliferation of CMs and significantly promoted the apoptosis and autophagy of CMs in HR.
CONCLUSIONS: Focusing on the protective effects of CUR and ECs on cardiomyocytes is of great significance for the treatment of clinical myocardial HR injury.
摘要：
目的：内皮细胞（ECs）可以通过分泌衍生因子为缺氧-复氧（HR）条件下的心肌细胞（CMs）提供细胞保护。本研究旨在探讨姜黄素(CUR)在ECs中保护CMs免受HR损伤的作用。
方法：建立了EC和CM的共培养系统，并服从HR。转录，表达式,通过RT-qPCR检测FGF2的分泌，westernblot,和ELISA，分别。将特异性靶向FGF2的siRNA转染到EC中。FGF2受体特异性抑制剂（AZD4547）用于治疗CM。
结果：与EC共培养不影响CM的增殖，而CUR和ECs共培养对促进HR中CMs增殖具有协同作用。此外，与EC共培养不影响HR中CM的凋亡和自噬。然而,CUR处理后的ECs共培养抑制了HR中CMs的凋亡和自噬。CUR处理显著增强FGF2mRNA，蛋白质，和HR中ECs的分泌水平。此外,CUR处理增加了EC和CM共培养系统中CM培养基中的FGF2水平。培养基中FGF2水平的降低和FGF2受体的抑制明显抑制了HR中CMs的增殖，并明显促进了CMs的凋亡和自噬。
结论：关注CUR和ECs对心肌细胞的保护作用对临床心肌HR损伤的治疗具有重要意义。
方法：建立了EC和CM的共培养系统，并服从HR。转录，表达式,通过RT-qPCR检测FGF2的分泌，westernblot,和ELISA，分别。将特异性靶向FGF2的siRNA转染到EC中。FGF2受体特异性抑制剂（AZD4547）用于治疗CM。
结果：与EC共培养不影响CM的增殖，而CUR和ECs共培养对促进HR中CMs增殖具有协同作用。此外，与EC共培养不影响HR中CM的凋亡和自噬。然而,CUR处理后的ECs共培养抑制了HR中CMs的凋亡和自噬。CUR处理显著增强FGF2mRNA，蛋白质，和HR中ECs的分泌水平。此外,CUR处理增加了EC和CM共培养系统中CM培养基中的FGF2水平。培养基中FGF2水平的降低和FGF2受体的抑制明显抑制了HR中CMs的增殖，并明显促进了CMs的凋亡和自噬。
结论：关注CUR和ECs对心肌细胞的保护作用对临床心肌HR损伤的治疗具有重要意义。
