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http://dx.doi.org/10.4014/jmb.0812.662

Baicalein Induces Programmed Cell Death in Candida albicans  

Dai, Bao-Di (School of Pharmacy, Second Military Medical University)
Cao, Ying-Ying (School of Pharmacy, Second Military Medical University)
Huang, Shan (School of Pharmacy, Second Military Medical University)
Xu, Yong-Gang (School of Pharmacy, Second Military Medical University)
Gao, Ping-Hui (School of Pharmacy, Second Military Medical University)
Wang, Yan (School of Pharmacy, Second Military Medical University)
Jiang, Yuan-Ying (School of Pharmacy, Second Military Medical University)
Publication Information
Journal of Microbiology and Biotechnology / v.19, no.8, 2009 , pp. 803-809 More about this Journal
Abstract
Recent evidence has revealed the occurrence of an apoptotic phenotype in Candida albicans that is inducible with environmental stresses such as acetic acid, hydrogen peroxide, and amphotericin B. In the present study, we found that the Chinese herbal medicine Baicalein (BE), which was one of the skullcapflavones, can induce apoptosis in C. albicans. The apoptotic effects of BE were detected by flow cytometry using Annexin V-FITC and DAPI, and it was confirmed by transmission electron microscopy analysis. After exposure to 4 ${\mu}g$/ml BE for 12 h, about 10% of C. albicans cells were apoptotic. Both the increasing intracellular levels of reactive oxygen species (ROS) and upregulation of some redox-related genes (CAP1, SOD2, TRR1) were observed. Furthermore, we compared the survivals of CAP1 deleted, wild-type, and overexpressed strains and found that Cap1p attenuated BE-initiated cell death, which was coherent with a higher mRNA level of the CAP1 gene. In addition, the mitochondrial membrane potential of C. albicans cells changed significantly (p<0.001) upon BE treatment compared with control. Taken together, our results indicated that BE treatment induced apoptosis in C. albicans cells, and the apoptosis was associated with the breakdown of mitochondrial membrane potential.
Keywords
Candida albicans; Baicalein; programmed cell death; mitochondrial membrane potential;
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