Our previous investigation suggested that faster seventh cervical nerve (C7) regeneration occurs in patients with cerebral injury undergoing contralateral C7 transfer. This finding needed further verification, and the mechanism remained largely unknown. Here, Tinel’s test revealed faster C7 regeneration in patients with cerebral injury, which was further confirmed in mice by electrophysiological recordings and histological analysis. Furthermore, we identified an altered systemic inflammatory response that led to the transformation of macrophage polarization as a mechanism underlying the increased nerve regeneration in patients with cerebral injury. In mice, we showed that, as a contributing factor, serum amyloid protein A1 (SAA1) promoted C7 regeneration and interfered with macrophage polarization in vivo. Our results indicate that altered inflammation promotes the regenerative capacity of the C7 nerve by altering macrophage behavior. SAA1 may be a therapeutic target to improve the recovery of injured peripheral nerves.

我们之前的研究表明，接受对侧 C7 移植的脑损伤患者的第七颈神经 (C7) 再生速度更快。这一发现需要进一步验证，而且其机制仍然很大程度上未知。在这里，蒂内尔的测试表明，脑损伤患者的 C7 再生速度更快，这一点通过电生理记录和组织学分析在小鼠身上得到了进一步证实。此外，我们发现全身炎症反应的改变导致巨噬细胞极化转变，这是脑损伤患者神经再生增加的潜在机制。在小鼠中，我们发现，作为一个促成因素，血清淀粉样蛋白 A1 (SAA1) 促进 C7 再生并干扰体内巨噬细胞极化。我们的结果表明，改变的炎症通过改变巨噬细胞的行为来促进 C7 神经的再生能力。 SAA1可能是改善受损周围神经恢复的治疗靶点。