Chen Nai-hong

SDF-1 α /CXCR4轴在干细胞治疗缺血性脑卒中的研究进展

脑卒中具有高发病率、高致残率和高死亡率的特点, 是目前导致我国居民死亡的首位病因, 其中缺血性卒中占据了脑卒中的87%, 但尚缺乏理想的治疗方法。干细胞是一类具有自我更新能力、高度分化潜能的细胞。干细胞移植可打破卒中后梗死区域难以恢复的传统观念。然而, 干细胞治疗缺血卒中需要特定的趋化因子诱导其定向迁移至损伤组织部位, 基质细胞衍生因子-1α(stromal cell-derived factor-1α, SDF-1α)即是典型代表之一。SDF-1α和其特异性受体CXCR4不仅可以诱导其定性迁移, 还能够增加干细胞增殖, 促进血管新生。本文就SDF-1α/CXCR4轴在干细胞治疗缺血性脑卒中的作用进行综述, 以期为提升干细胞移植治疗缺血性脑卒中的疗效提供理论基础。

人参皂苷Rg1调控miR-153/Nrf2/HO-1减轻肌萎缩侧索硬化模型小鼠损伤

本文主要通过肌萎缩侧索硬化症（amyotrophic lateral sclerosis，ALS）模型小鼠（SOD1 G93A）研究人参皂苷Rg1对ALS病程及病理的影响，并对其作用机制进行分析。通过体重及生存率监测小鼠病程，转棒实验测试小鼠肌肉运动协调能力，甲苯胺蓝染色及免疫荧光检测小鼠脊髓运动神经元及小胶质细胞改变，Western blot检测氧化应激相关蛋白Nrf2等的表达，并对其及相关miRNA进行干预，验证Rg1的作用及相关机制。结果显示20 mg·kg-1·d-1 Rg1可明显延缓ALS小鼠病程，改善其运动症状，减少脊髓运动神经元丢失并抑制小胶质细胞激活。进一步研究发现Rg1通过抑制ALS小鼠脊髓miR-153表达，解除其对Nrf2转录后抑制，使其表达明显上调，进而激活HO-1抗氧化信号通路。本研究表明Rg1通过调节miR-153/Nrf2/HO-1抗氧化损伤，对ALS小鼠发挥神经保护作用，为将Rg1开发为有效的ALS治疗药物提供理论依据。

Protein kinase-based neural signaling pathways for ginsenosides: a retrospective review

Ginsenosides are the main active components of ginseng, which have been reported to target brain tissues and produce multiple neuroprotective effects. Ginsenosides have been shown to improve learning ability and memory in normal aged animals, and in an animal model of memory impairment. However, its underlying pharmacological mechanisms are very complicated, especially with regard to its effects on the activation of protein kinases in neurons. Previous reports have shown that some protein kinases may be affected by ginsenosides, including protein kinase C, calcium/calmodulin-dependent protein kinase II, c-Jun-N terminal kinase, and protein tyrosine kinase. In this paper, protein kinases that may underlie the mechanisms of ginsenosides will be discussed.