Article Publish Status: FREE
Abstract Title:

Carvacrol InducesApoptosis Associated With Ca/Calcineurin Pathway.

Abstract Source:

Front Cell Infect Microbiol. 2020 ;10:192. Epub 2020 Apr 30. PMID: 32426298

Abstract Author(s):

Chao Niu, Chenglu Wang, Yijia Yang, Ruiyao Chen, Jian Zhang, Haiyan Chen, Yingzhi Zhuge, Jingqi Li, Jianhua Cheng, Ke Xu, Maoping Chu, Chunhua Ren, Chunxiang Zhang, Chang Jia

Article Affiliation:

Chao Niu


As the prevalence of systemic fungal infections caused bygradually increases, it is necessary to explore potential and effective antifungals. Carvacrol is reported to be lethally toxic to, involving several potential mechanisms. However, the form and specific mechanism of cell death caused by this compound has not been delineated. In this study, we found that carvacrol could significantly decreasesurvival rates, consistent with previous researches. Further examination proved that carvacrol treatment caused cell membrane permeability and depolarization. To elucidate the association between cell death and apoptosis, DNA fragmentation and metacaspase activation were determined; as expected, these two apoptosis-related markers were clearly observed. Moreover, total and mitochondrial reactive oxygen species (ROS) levels were elevated, and both mitochondrial transmembrane potential and morphology were disrupted. Additionally, cytosolic and mitochondrial calcium levels were also increased by carvacrol. Calcineurin inhibition experiments revealed cyclosporine A (CsA) addition notably rescued cell growth and inhibited metacaspase activation, indicating that carvacrol triggeredapoptosis through inducing calcineurin activation. Carvacrol was demonstrated to both have low toxicity and be effective in alleviating systemic infections with, which might be via its antifungal and immunomodulation activities. This study suggests that carvacrol has excellent potential as a natural protective compound againstinfections.

Study Type : In Vitro Study

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