摘要
多氯联苯(PCB)引发子宫内膜异位症(内异症)的分子机制尚不明确.文章分析了PCB31对原代培养的异位内膜基质细胞的影响.结果显示:低浓度PCB31不影响细胞增殖,而高浓度则抑制细胞增殖.PCB31增强基质金属蛋白酶MMP2和环加氧酶COX-2的表达,白介素IL1β和IL8的表达也上调.酶联免疫结果也证实PCB31上调白介素的分泌.综合以上,PCB31可通过上调发病相关基因的表达从而影响内异症.
The molecular mechanism of polychlorinated biphenyls （PCB） on endometriosis was still un- known. This study aimed to assess the effects of PCB31 on endometriotic stromal cells derived from primary culture. The results showed that lower concentrations of PCB31 did not affect the proliferation while higher concentration inhibited the proliferation. The mRNA expression of the matrix metalloproteinase （MMP2） gene and the cyclooxygenase-2 （COX-2） gene was both up- regulated after PCB31 exposure. PCB31 induced the expression of interleukin both at the mRNA and protein level. In all, PCB31 could affect endometriosis through up-regulation of related genes.
出处
《泉州师范学院学报》
2013年第6期1-4,8,共5页
Journal of Quanzhou Normal University
基金
福建省自然科学基金(2011J05117)
国家自然科学基金(21107107)
关键词
多氯联苯
子宫内膜异位症
白介素
基质金属蛋白酶
polychlorinated biphenyls, endometriosis, interleukin, matrix metalloproteinase
