Human umbilical cord-derived mesenchymal stem cell (hUC-MSC) transplantation is thought to be a promising strategy for treating spinal cord injury (SCI). However, the low survival rate of transplanted hUC-MSCs limits their clinical application in cell replacement therapy. Curcumin can suppress inflammation after SCI; however, it remains unknown whether curcumin can modulate the survival of transplanted hUC-MSCs. In this study, to investigate whether curcumin could strengthen the therapeutic effects of hUC-MSC transplantation on SCI, we induced hUC-MSC apoptosis with TNF-α, transplanted hUC-MSC into SCI rats, and assessed the antiapoptotic effect and mechanism of curcumin. LDH release analysis and flow cytometry demonstrated that TNF-α led to hUC-MSC apoptosis and that curcumin increased the hUC-MSC survival rate in a dose-dependent manner. In addition, we showed that the phosphorylation levels of ERK1/2, JNK, and P38 were upregulated in apoptotic hUC-MSCs, while curcumin increased the phosphorylation of ERK1/2 but did not activate JNK or P38, and these effects were reversed by the p42/44 antagonist U0126. Furthermore, we found that the motor function scores and number of surviving HNA-positive cells were significantly increased after curcumin and hUC-MSC transplantation therapy 8 weeks post-SCI, while U0126 markedly attenuated these effects. These data confirmed that curcumin suppressed hUC-MSC apoptosis through the ERK1/2 signaling pathway and that combined curcumin and hUC-MSC treatment improved motor function in rats after SCI. The current research provides a strong basis for hUC-MSC replacement therapy in conjunction with curcumin in the treatment and management of SCI in humans.

人脐带间充质干细胞 (hUC-MSC) 移植被认为是治疗脊髓损伤 (SCI) 的一种有前途的策略。然而，移植的 hUC-MSCs 的低存活率限制了它们在细胞替代疗法中的临床应用。姜黄素可以抑制 SCI 后的炎症；然而，姜黄素是否可以调节移植的 hUC-MSCs 的存活仍然未知。在本研究中，为了探讨姜黄素是否可以增强 hUC-MSC 移植对 SCI 的治疗作用，我们用 TNF-α 诱导 hUC-MSC 凋亡，将 hUC-MSC 移植到 SCI 大鼠体内，并评估姜黄素的抗凋亡作用和机制。LDH 释放分析和流式细胞术表明 TNF-α 导致 hUC-MSC 凋亡，姜黄素以剂量依赖性方式提高 hUC-MSC 存活率。此外，我们发现 ERK1/2、JNK 和 P38 的磷酸化水平在凋亡的 hUC-MSCs 中上调，而姜黄素增加了 ERK1/2 的磷酸化但不激活 JNK 或 P38，这些作用被逆转p42/44 拮抗剂 U0126。此外，我们发现姜黄素和 hUC-MSC 移植治疗脊髓损伤后 8 周后，运动功能评分和存活的 HNA 阳性细胞数量显着增加，而 U0126 显着减弱了这些影响。这些数据证实姜黄素通过 ERK1/2 信号通路抑制 hUC-MSC 凋亡，姜黄素和 hUC-MSC 联合治疗可改善 SCI 后大鼠的运动功能。