研究p300乙酰化在卡介苗(bacillus Calmette-Guérin,BCG)感染中的作用。构建THP-1巨噬细胞模型,比较BCG感染前后p300蛋白表达水平和组蛋白H3乙酰化水平的改变,加入p300特异性抑制剂Delphinidin,观察细胞内组蛋白H3乙酰化水平的变化。结果表明,在分化成熟的THP-1细胞系中,BCG感染能够上调p300蛋白表达水平和组蛋白H3乙酰化水平,加入p300特异性抑制剂Delphinidin后,组蛋白H3乙酰化水平降低。BCG感染通过p300途径导致蛋白质乙酰化水平发生改变。
The role of p300 acetylation of BCG ( bacillus, Calmette-Gu6rin) infection was studied. THP-1 macro- phage model was constructed to compare the changes of the expression level of p300 protein and histone H3 acetylation level before and after BCG infection, adding p300 specific inhibitor of delphinidin, and observe the changes of acety- lation level in H3 histone. The results showed that in a mature differentiation of THP-1 cell system, the BCG infection could up regulated the protein expression level of p300 and histone H3 acetylation level, and after adding p300 specif- ic inhibition preparation of delphinidin, the level of histone H3 acetylation reduced. Therefore, BCG infection may lead to the change of protein acetylation level through p300 pathways.