摘要
目的:探讨维生素D(VD)通过自噬通路减轻实验性变态反应性脑脊髓炎(EAE)小鼠神经功能损伤的影响。方法:将6~8周的雌性C57BL/6及同源Atg5(+/-)小鼠各12只,分别随机分4组各6只,A组为C57BL/6小鼠+蓖麻油,B组为C57BL/6小鼠+1,25(OH)_(2)D_(3),C组为Atg5(+/-)小鼠+蓖麻油,D组为Atg5(+/-)小鼠+1,25(OH)_(2)D_(3)。在造模后20天处死小鼠,留取其脑组织、脊髓、脾脏,通过临床评分,酶联免疫吸附测定等方法,观察VD对两种小鼠EAE模型神经组织损伤程度、炎症相关指标以及自噬相关指标的影响。结果:到取材为止,A、C、D组小鼠发病率为100%,B组发病率为11.1%。自第11天起,B组小鼠的神经功能评分明显低于A、C、D组(均P<0.05)。B组的IFN-γ、TNF-α、IL-17表达低于A、C、D组,TGF-β、IL-4表达高于A、C、D组(均P<0.05)。B组的Atg5蛋白水平高于A组,LC3蛋白水平低于A、B、C组;B组的LC3 mRNA表达量低于A、C、D组(P<0.05)。结论:VD可以通过调节自噬基因的表达介导保护神经,其有望成为治疗多发性硬化症(MS)的新方向。
Objective:To explore the effect of vitamin D(VD)through the autophagy pathway to reduce the neurological damage in mice with experimental allergic encephalomyelitis(EAE).Methods:6-8 weeks old female C57BL/6 and homologous Atg5(+/-)mice were randomLy divided into 4 groups with 6 mice each,group A was C57BL/6 mice+castor oil,group B It is C57BL/6 mouse+1,25(OH)_(2)D_(3),group C is Atg5(+/-)mouse+castor oil,group D is Atg5(+/-)mouse+1,25(OH)_(2)D_(3).The mice were sacrificed 20 days after modeling,and their brain tissue,spinal cord,and spleen were collected.Through clinical scoring,enzyme-linked immunosorbent assay and other methods,the VD's damage to the nerve tissue,inflammation-related indicators and indicators of the two EAE models of mice were observed.The impact of autophagy-related indicators.Results:Up to the time the material was collected,the incidence of mice in groups A,C,and D was 100%,and the incidence in group B was 11.1%.From the 11th day,the neurological scores of mice in group B were significantly lower than those in groups A,C,and D(all P<0.05).The expressions of IFN-γ,TNF-α and IL-17 in group B were lower than those in groups A,C and D,and the expression of TGF-β and IL-4 were higher than those in groups A,C and D(all P<0.05).The Atg5 protein level of group B was higher than that of group A,and the protein level of LC3 was lower than that of group A,B,and C;the expression of LC3 mRNA in group B was lower than that of group A,C,and D(P<0.05).Conclusion:VD can mediate the protection of nerves by regulating the expression of autophagy genes,and it is expected to become a new direction for the treatment of multiple sclerosis(MS).
作者
陈培材
廖伟锋
饶俊平
Chen Peicai(Department of Neurology,Yuedong Hospital,Third Affiliated Hospital of Sun Yat-Sen University,Meizhou Guangdong 514000)
出处
《黑龙江医药》
CAS
2022年第2期254-257,共4页
Heilongjiang Medicine journal
基金
2018年度梅州市社会发展科技计划项目(项目编号:2018B118)。
