人参环氧炔醇对雪旺细胞神经保护作用的影响及机制

Effect and mechanisms of panaxydol upon Schwann cells neuroprotection

目的：研究人参环氧炔醇（PND）对体外培养雪旺细胞（SCs）保护过氧化氢（Hz02）损伤的大鼠皮层神经元的作用并探讨其作用机制。方法：在培养1周的小鼠皮层神经元培养基中加入H202，建立神经元氧化损伤模型，与以PND（10／μmol／L）预处理体外培养SCs共培养，用CCK-8法检测细胞活力，ELISA检测突触素（synaptophysin，SYN）水平，共聚焦显微镜观察突触及细胞骨架；实时荧光定量-PCR、RT-PCR检测神经元凋亡相关基因bcl-2、bax的表达，进行图像处理及统计分析。结果：与正常组相比，H2O2组细胞存活率降低。与Hzoz组相比，PND（10μmol／L）组、SCs组及PND（10μmol／L）预处理SCs组细胞存活率升高，并且bcl-2mRNA表达上调、baxmRNA表达下调，各指标差异均有统计学意义，而以PND（10μmol／L）预处理SCs组作用最显著。结论：PND可促进SCs对H。02所致皮层神经元损伤的保护作用，其机制可能与PND预处理的SCs调节皮层神经元的细胞凋亡相关蛋白表达从而抑制凋亡有关。

Objective： To study the protective effects of panaxydol （PND） treated with Schwann cells （SCs） while co-cul- tured with H2O2 injured cortical neurons. Methods： An oxidative injury model of the neurons induced by H2O2 in mice was co-cultured with Schwann cells pretreated with 10μmol/L PND： The cell viability was detected by CCK-8. The content of synaptophysin （SYN）, cytoskeleton and cellular morphology in the neurons were detected after being treated with different methods. Meanwhile the mRNA expression of bcl-2 and bax was quantified by QRT-PCR and RT-PCR. Results： H2O2 could induce oxidative injury in the neurons, and decreased the cell viability. Compared with H2O2 group, the levels of the cell viability and SYN expression were increased in Schwann cells group, 10μmol/L PND group and Schwann cells pretreated with 10/zmol/L PND group. In addition, the mRNA expression of hcl-2 increased and that of bax decreased in Schwann cells group, 10μmol/L PND group and Sehwann cells pretreated with 10 pmol/L PND group and peaked in Schwann cells pretreated with 10 μmol/L PND group. Conclution： The protective effect d Schwann ceils pretreated with 10μmol/L PND on the neurons with Hz Oz-induced injury may be involved in the mechanisms of the regulation of Bcl-2 family and suppression of bax activity.