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作 者:李涛[1] 唐礼江[1] 徐晨凯[1] 许莎莎[1] 江建军[1] 方崇峰[1] 王斌[1] 卢先本[1]
机构地区:[1]温州医学院附属台州医院心内科,临海317000
出 处:《医学研究杂志》2013年第4期78-81,共4页Journal of Medical Research
基 金:浙江省医药卫生科技计划项目(2011ZDA028)
摘 要:目的探讨白三烯B4在MAPK信号通路中对细胞外基质金属蛋白酶诱导因子(EMMPRIN)表达的影响。方法将人类单核细胞系THP-1分为6组,用PMA诱导2~6组的THP-1成巨噬细胞,3~6组加入白三烯B4,第4组加入PD98059(ERK1/2抑制剂),第5组加入SB203580(P38抑制剂),第6组加入SP600125(JNK抑制剂),观察EMMPRIN和MMP-9的mR-NA以及EMMPRIN的蛋白变化。结果 LTB4使单核细胞EMMPRIN的mRNA表达增加(P<0.05)、MMP-9的mRNA表达增加(P<0.01),及EMMPRIN的蛋白表达明显增加(P<0.01),加入PD98059后,EMMPRIN的mRNA表达明显下降(P<0.01),MMP-9的mRNA表达明显下降(P<0.01),EMMPRIN蛋白表达明显下降(P<0.01),加入SB203580后,EMMPRIN的mRNA明显下降(P<0.01),MMP-9的mRNA明显下降(P<0.01),EMMPRIN蛋白表达明显下降(P<0.01),加入SP600125后,EMM-PRIN的mRNA明显下降(P<0.05),MMP-9的mRNA明显下降(P<0.01),EMMPRIN蛋白表达明显下降(P<0.01)。结论白三烯B4通过激活MAPK信号通路增加THP-1源性巨噬细胞EMMPRIN的表达,可能是其增加巨噬细胞MMPs产生的机制。Objective To investigate the effect of LTB4 on EMMPRIN expression via MAPK pathway of macrophages. Methods THP - 1 cells were incubated in 6 - well culture plates and divided into six groups. These cells were correspondingly pretreated with PMA ( 2 - 6groups) then incubated with LTB4 ( 3 - 6groups) and PD98059 (4group) , SB203580 ( 5 group) , SP600125 (6group) , To observe the expression of EMMPRIN and MMP -9 on mRNA and the expression of EMMPRIN on protein. Results LTB4 up - regulated the expres- sion of EMMPRIN on mRNA(P〈0.05),MMP-9 on mRNA(P〈O.01), EMMPRIN on protein(P〈0.01).PD98059(or PD, which is a specific MEK/ERK inhibitor) suppress the up- regulation of EMMPRIN on mRNA(P 〈0.01 ),MMP-9 on mRNA(P 〈0.01 ),EMM- PRIN on protein (P 〈 0.01 ) , SP600125 ( or SP, which is a specific Jun N - terminal kinase inhibitor, JNK) suppress the up - regulation of EMMPRIN on mRNA(P 〈0.01 ) ,MMP -9 on mRNA(P 〈0.01 ) ,EMMPRIN on protein(P 〈0.01 ) ,SB203580 (or SB, which is a spe- cific p38/MAPK inhibitor) suppress the up - regulation of EMMPRIN on mRNA ( P 〈 0.05 ) , MMP - 9 on mRNA ( P 〈 0.01 ) , EMMPRIN on protein(P 〈 0.01 ). Conclusion EMMPRIN expression is greatly up - regulated by LTB4 via MAPK pathway. LTB4 may be the un- derlying mechanism of its stimulation effect on MMP- 9 production by macrophages.
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