CSCI诱导的脱髓鞘病变后电针对髓鞘再生的修复作用及其机制研究

Demyelination induced by compressed spinal cord injury(CSCI)would lead to serious neurological function disorders which impair patients'health.Acupuncture therapy is effective in the treatment of spinal cord injury.In our previous studies,the results achieved are as follows:demyelination was induced by CSCI;oligodendrocyte that is myelinforming cell in central nervous system underwent apoptosis ;Id2 was overexpressed in oligodendrocyte and MBP expression was downregulation.The oligodendrocyte apoptosis and the alterations of Id2 and MBP expressions may contribute to demyelination after CSCI.The further experiment proved that electroacupuncture stimulation induced OPCs proliferation,downregulation of Id2 and upregulation of MBP.The results showed that electroacupuncture can help injured spinal cord recovery.However, the effect of electroacupuncture on remyelination and underlying molecular mechanism of electroacupuncture in proliferation and differentiation of OPCs remain to be explored.Therefore, it is necessary for us to do further study to verify it.. The protocols are designed as follows: A custum-made of compressed spinal cord injury in rats is established.Pathological changes of demyelination after CSCI, the effect of electroacupuncture on remyelination and mechanism of electroacupuncture therapy in proliferation and differentiation of OPCs are investigated by the methods of transmission electronic microscope,confocal laser,western blotting,PCR,and EMSA. And then,the data are analyzed,so as to clarify the mechanism of demyelination,the influence of electroacupuncture therapy on spinal cord nervous function recovery,as well as the mechanism of electroacupuncture therapy in treatment of axonal demyelination induced by CSCI.The results can provide the experimental basis for electroacupuncture therapy to treat the CSCI in clinic.

脊髓压迫性损伤(CSCI) 诱导的脱髓鞘病变将导致严重的神经功能障碍，危害患者的身体健康。针灸疗法对脊髓损伤的康复治疗具有确切的疗效。本课题组前期工作发现：CSCI可诱导脊髓脱髓鞘病变；该病变与脊髓少突胶质细胞凋亡、少突胶质细胞转录因子Id2表达升高、髓鞘主要结构蛋白MBP表达下调有关。预实验结果表明：电针刺激后，少突胶质前体细胞（OPCs）有增殖、Id2表达下调、MBP表达升高，提示电针对脱髓鞘病变有修复作用。然而，电针在促进OPCs的增殖、分化，髓鞘再生中的作用及其分子机制尚不清楚，还需进一步研究。为此，本项目拟采用自行研制并取得专利 (ZL:200520009289X）的大鼠CSCI模型，通过透射电镜、激光共聚焦、免疫印迹、PCR、EMSA等分子生物学技术，对CSCI后脱髓鞘病变机制、电针对CSCI髓鞘再生的作用及其机制进行研究。为针灸临床治疗CSCI提供实验基础和理论依据。

项目背景：脊髓压迫性损伤 后，脊髓白质发生脱髓鞘病变，是导致神经功能障碍的主要原因之一。如未能及时治疗，将导致不可逆的功能缺失，对患者的身心健康造成严重的伤害 。因此，对CSCI诱导的脱髓鞘病变机制及其治疗的研究具有十分重要的意义。.主要研究内容：本项目在制作CSCI模型的基础上，采用透射电镜、激光共聚焦、免疫印迹等分子生物学技术，从CSCI诱导的脱髓鞘病变机制以及电针对CSCI脱髓鞘病变保护的作用机制两方面进行了研究。.重要结果及关键数据显示：电针可提高脊髓损伤大鼠的运动功能评分以及髓鞘修复，电针组里增殖的少突胶质前体细胞和少突胶质细胞比对照组明显增 多，Olig2蛋白表达水平随时间延长均逐渐增加，Id2表达逐渐下降；并通过抑制凋亡因子caspase-12 和 cytochrome c的表达，促进MBP 的水平增高。.科学意义：电针治疗脊髓损伤疗效显著，其机制可能与促进少突胶质细胞增殖，抑制少突胶质细胞凋亡有关。该项目可为针灸临床治疗CSCI提供实验基础和理论依据