School of Pharmacy, Henan University, Kaifeng 475001, People's Republic of China; Key Laboratory of Natural Medicine and Immune Engineering, Henan University, Kaifeng 475001, People's Republic of China.
Key Laboratory of Natural Medicine and Immune Engineering, Henan University, Kaifeng 475001, People's Republic of China.
Neuroscience. 2018 Jan 15;369:314-324. doi: 10.1016/j.neuroscience.2017.11.027. Epub 2017 Nov 24.
Accumulated evidence displayed that transplantation of stem cells may be a promising approach for the treatment of neurological disorders. However, the underlying mechanisms remain to be well elucidated. Moreover, some investigators cannot reproduce similar results as the previous. The present results showed that transplantation of fresh human umbilical cord blood mononuclear cells (cbMNCs) attenuated ischemic damage in middle cerebral artery occlusion (MCAO) rats, accompanied with improvement of neurologic deficits, learning and memory function. The increase in neovascularization and related molecules such as vascular endothelial growth factor (VEGF), Angiopoietin-1 (Ang-1) and endothelium-specific receptor tyrosine kinase 2 (Tie-2) in the injured brain was observed in cbMNCs-treated rats. Moreover, nuclear factor-κB (NF-κB) activation and nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome were also inhibited by the cells graft, resulting in reduction in cleaved caspase-1 and mature interleukin-1β (IL-1β) content. These results suggested that the protective actions of the cells on the cerebral ischemia may be related to inhibition of NF-κB pathway and NLRP3 inflammasome.
越来越多的证据表明，干细胞移植可能是治疗神经紊乱的一种有前途的方法。然而，其潜在机制仍有待阐明。此外，一些研究人员无法复制与之前相似的结果。本研究结果表明，新鲜人脐带血单个核细胞（cbMNCs）移植减轻了大脑中动脉闭塞（MCAO）大鼠的缺血性损伤，伴随着神经功能缺损、学习和记忆功能的改善。在 cbMNCs 治疗的大鼠受损大脑中观察到血管生成和相关分子（如血管内皮生长因子（VEGF）、血管生成素-1（Ang-1）和内皮细胞特异性受体酪氨酸激酶 2（Tie-2））的增加。此外，移植的细胞还抑制了核因子-κB（NF-κB）的激活和核苷酸结合和寡聚化结构域样受体家族吡咯烷结构域包含 3（NLRP3）炎症小体，从而减少了裂解的半胱天冬酶-1 和成熟的白细胞介素-1β（IL-1β）的含量。这些结果表明，细胞对脑缺血的保护作用可能与抑制 NF-κB 通路和 NLRP3 炎症小体有关。
