ArticlePloS one2017
Honokiol induces reactive oxygen species-mediated apoptosis in Candida albicans through mitochondrial dysfunction.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 107 citations in OpenAlex.
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- Decreased expression ofAmerican journal of clinical and experimental urology · 2024Article
- Honokiol induces apoptosis-like death in Cryptocaryon irritans Tomont.Parasites & vectors · 2023Article
- Antifungal activity of Allyl isothiocyanate by targeting signal transduction pathway, ergosterol biosynthesis, and cell cycle inCurrent medical mycology · 2023Article
- Curcumin-Functionalized Graphene Oxide Strongly PreventsPharmaceuticals (Basel, Switzerland) · 2023Article
- Physiological and transcriptome analysis ofFrontiers in cellular and infection microbiology · 2023Article
- Sphingosine as a New Antifungal Agent againstInternational journal of molecular sciences · 2022Article
- Inhibitory Effects and Mechanism of Action of Elsinochrome A onJournal of fungi (Basel, Switzerland) · 2022Article
- The application prospects of honokiol in dermatology.Dermatologic therapy · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the effects of honokiol on induction of reactive oxygen species (ROS), antioxidant defense systems, mitochondrial dysfunction, and apoptosis in Candida albicans.
methodsTo measure ROS accumulation, 2',7'-dichlorofluorescein diacetate fluorescence was used. Lipid peroxidation was assessed using both fluorescence staining and a thiobarbituric acid reactive substances (TBARS) assay. Protein oxidation was determined using dinitrophenylhydrazine derivatization. Antioxidant enzymatic activities were measured using commercially available detection kits. Superoxide dismutase (SOD) genes expression was measured using real time RT-PCR. To assess its antifungal abilities and effectiveness on ROS accumulation, honokiol and the SOD inhibitor N,N'-diethyldithiocarbamate (DDC) were used simultaneously. Mitochondrial dysfunction was assessed by measuring the mitochondrial membrane potential (mtΔψ). Honokiol-induced apoptosis was assessed using an Annexin V-FITC apoptosis detection kit.
resultsROS, lipid peroxidation, and protein oxidation occurred in a dose-dependent manner in C. albicans after honokiol treatment. Honokiol caused an increase in antioxidant enzymatic activity. In addition, honokiol treatment induced SOD genes expression in C. albicans cells. Moreover, addition of DDC resulted in increased endogenous ROS levels and potentiated the antifungal activity of honokiol. Mitochondrial dysfunction was confirmed by measured changes to mtΔψ. The level of apoptosis increased in a dose-dependent manner after honokiol treatment.
conclusionsCollectively, these results indicate that honokiol acts as a pro-oxidant in C. albicans. Furthermore, the SOD inhibitor DDC can be used to potentiate the activity of honokiol against C. albicans.
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