Baicalein induces programmed cell death in Candida albicans

Area of Science:

• Mycology
• Pharmacology
• Cell Biology

Background:

• Candida albicans exhibits an inducible apoptotic phenotype under environmental stress.
• Chinese herbal medicines are explored for novel therapeutic agents.

Purpose of the Study:

• To investigate the potential of Baicalein (BE), a skullcapflavone, to induce apoptosis in Candida albicans.
• To elucidate the mechanisms underlying BE-induced apoptosis in C. albicans.

Main Methods:

• Flow cytometry with Annexin V-FITC and DAPI staining.
• Transmission electron microscopy.
• Analysis of reactive oxygen species (ROS) levels and redox-related gene expression (CAP1, SOD2, TRR1).
• Comparative survival assays of C. albicans strains with altered CAP1 expression.
• Assessment of mitochondrial membrane potential.

Main Results:

• Baicalein (4 microg/ml for 12 h) induced apoptosis in approximately 10% of C. albicans cells.
• BE treatment led to increased intracellular ROS levels and upregulation of CAP1, SOD2, and TRR1.
• Deletion of CAP1 exacerbated BE-induced cell death, while overexpression conferred protection.
• Significant disruption of mitochondrial membrane potential was observed in BE-treated cells.

Conclusions:

• Baicalein effectively induces apoptosis in Candida albicans.
• The apoptotic process is linked to increased ROS production and mitochondrial membrane potential breakdown.
• The redox regulator Cap1p plays a role in modulating the sensitivity to Baicalein-induced cell death.