Investigation on the induction mechanism of hepatocyte death by fungal reactive oxygen species

白色念珠菌CaCFL11在与肝细胞共培养下表达增强，产生ROS，引起肝细胞凋亡现象。我们构建了与GFP融合的CaCFL11基因启动子杂合突变体。这些突变体的结果表明，CaCFL11的表达在与肝细胞共培养的反应中受到调节，并有助于靶向参与CaCFL11表达的转录因子的结合区。另一方面，天然产物姜黄素作为一种候选药物已被广泛研究，并显示出抗白色念珠菌的活性。我们的抗真菌耐药研究表明，姜黄素影响白色念珠菌热休克蛋白90 （Hsp90）的功能和多药转运蛋白Cdr1的药物外排泵活性。

Candida albicans CaCFL11 showed enhanced expression under the co-culture with hepatic cells, resulting in ROS production and cause hepatocytes apoptosis phenomenon. We constructed heterozygous mutants of CaCFL11 gene promoter fused to GFP. The results from these mutants indicated CaCFL11 expression was regulated in response to co-culture with hepatocytes and helped to target the binding region of transcription factors involved in the CaCFL11 expression. On the other hand, the natural product curcumin has been widely studied as a drug candidate and exhibited antifungal activity against C. albicans. Our study on antifungal drug resistance showed curcumin affected the function of heat shock protein 90 (Hsp90) and drug efflux pump activity of multidrug transporter protein Cdr1 in C. albicans.