C1q/tumor necrosis factor-related protein-3 (CTRP3) had shown its angiogenesis and enhancement of mitochondrial biogenesis properties in the treatment of myocardial infarction, but its potential roles in cerebral ischemic stroke had not been fully understood. This study aimed to clarify the underlying mechanism of how CTRP3 regulated mitochondrial functions in hippocampal neuronal cells (HPPNCs) after oxygen-glucose deprivation (OGD)/reoxygenation (R) treatment. Results showed that impeded CTRP3 expression and weakened viability were detected in OGD/R treated HPPNCs. CTRP3 showed its ability to enhance the viability and inhibited apoptosis of HPPNCs after OGD/R treatment and it could also promote the mitochondrial biogenesis and physiological functions. Silencing of PGC-1α partially abolished the protective function of CTRP3 on mitochondria and CTRP3 mediated the expression of PGC-1α via the AMPK/SIRT1-PGC-1α pathway. These findings provided information that CTRP3 prevented mitochondria from OGD/R injury through activating the AMPK/SIRT1-PGC-1α pathway. Our study suggested that CTRP3 might have the potential to become an emerging protective agent applied in the reperfusion treatment of ischemic stroke.

C1q /肿瘤坏死因子相关蛋白3（CTRP3）在治疗心肌梗塞中显示其血管生成和线粒体生物合成特性的增强，但其在脑缺血性中风中的潜在作用尚未得到充分了解。这项研究旨在阐明在氧葡萄糖剥夺（OGD）/复氧（R）处理后，CTRP3如何调节海马神经元细胞（HPPNC）的线粒体功能的潜在机制。结果表明，在OGD / R处理的HPPNC中检测到CTRP3表达受阻，并且活力减弱。CTRP3在OGD / R处理后显示出增强HPPNC活力并抑制其凋亡的能力，并且还可以促进线粒体的生物发生和生理功能。PGC-1α的沉默部分消除了CTRP3对线粒体的保护功能，而CTRP3通过AMPK /SIRT1-PGC-1α途径介导了PGC-1α的表达。这些发现提供了信息，表明CTRP3通过激活AMPK /SIRT1-PGC-1α途径防止线粒体受到OGD / R损伤。我们的研究表明CTRP3可能有潜力成为缺血性中风再灌注治疗中应用的新兴保护剂。