摘要
为探索维生素D对肠道先天免疫抗菌肽——α-防御素1(alpha-1-defensin,DEFA1)剪切酶基质金属蛋白酶7(matrix metalloproteinase 7,MMP-7)的调控,利用维生素D受体基因敲除小鼠(Vitamin D receptor knock-out,VDR-KO)与肠道细胞系作为研究模型,通过免疫组化染色、q RT-PCR及免疫印迹等研究方法,发现其肠道细胞中MMP-7的转录水平与蛋白水平较野生型(wild type,WT)小鼠显著降低,并且DEFA1的表达量也较低,表明维生素D可以调控肠道MMP-7的表达,从而影响DEFA1的成熟。同时,体外细胞实验表明:1,25-二羟基维生素D_3能够上调肠道细胞MMP-7的转录水平和蛋白水平。初步表明,维生素D通过调控MMP-7的表达影响DEFA1的成熟,而维生素D缺失,MMP-7下调从而DEFA1下调,进一步可能造成肠道菌群失调,导致多种慢性疾病的发生。
The aim of this study was to find the role of VD in regulating the active form of α-defensin 1 （DEFA1）, one of the antibacterial peptides in mouse intestine. It showed that the active DEFA1 was much lower in VDR knock-out mice compared to the wild type （WT） mice. Both mRNA and protein of matrix metalloproteinase-7 （MMP-7）, the cleaved enzyme of DEFA1, as detected by immumohistochemical staining and qRT-PCR, were at a relatively low level. In vitro experiment showed that VD can induce the expression of MMP-7 in colon cells. Thus, it suggested that VD can regulate the expression of MMP-7. When VD was deficient, MMP-7 was down-regulated and so was the active form of DEFA1, it might lead to impairment of intestinal innate immunity and dysbiosis and drive chronic disorders.
出处
《中国测试》
CAS
北大核心
2016年第8期57-63,共7页
China Measurement & Test
