论文部分内容阅读
目的:研究Smad相互作用蛋白1(Sip1)在cuprizone诱导髓鞘损伤再生模型中的表达变化及其意义。方法:通过在饲料中掺入cuprizone喂食C57BL/6小鼠建立髓鞘损伤模型,利用黑金(black gold,BG)染色方法及Western Blot方法,检测髓鞘损伤模型是否建立成功;利用Western Blot方法检测在髓鞘损伤及再生过程中Sip1的表达情况。结果:BG染色方法检测到喂药6周后模型组小鼠与对照组相比,着色显著降低,Western Blot方法检测到模型组小鼠MOG(myelin oligodendrocyte glycoprotein)蛋白表达水平显著降低,GFAP(glial fibrillary acidic protein)蛋白表达水平显著增高,证明髓鞘损伤模型建立成功。在模型建立成功后,停止喂药,改用正常饲料喂养4周后,通过Western Blot检测到模型组小鼠MOG蛋白水平显著恢复,证明该阶段髓鞘已再生。利用Western Blot方法检测髓鞘损伤模型建立阶段及髓鞘再生阶段的Sip1蛋白水平,结果显示与对照组小鼠相比,在髓鞘损伤阶段,模型组小鼠的Sip1蛋白水平显著增加,在髓鞘再生阶段Sip1蛋白水平同样显著增加。结论:Sip1在髓鞘损伤再生过程中具有重要作用,本研究为Sip1作为治疗髓鞘相关疾病的靶点提供了理论依据。
Objective: To investigate the expression of Smad-interacting protein 1 (Sip1) in cuprizone-induced remyelination injury model and its significance. Methods: The myelin sheath injury model was established by feeding cuprizone into the diet of C57BL / 6 mice. The myelin damage model was established by using black gold (BG) staining and Western Blot method. Western Blot Sip1 expression during myelin injury and regeneration. Results: After staining for 6 weeks, the expression of MOG (myelin oligodendrocyte glycoprotein) in model group was significantly lower than that in control group after 6 weeks of feeding. The expression of glial fibrillary acidic protein protein expression was significantly increased, indicating that myelin damage model was established. After the successful establishment of the model, the drug was stopped and fed to the normal diet for 4 weeks, the level of MOG protein in the model group was significantly recovered by Western Blot, indicating that the myelin has been regenerated at this stage. Western Blot method was used to detect the level of Sip1 protein during the establishment of myelin sheath injury and remyelination. The results showed that compared with the control group, the level of Sip1 protein in the model group increased significantly, Sip1 protein levels also increased significantly during the sheath regeneration phase. CONCLUSIONS: Sip1 plays an important role in the regeneration of myelin injury. This study provides a theoretical basis for Sip1 as a target for treatment of myelin-related diseases.