期刊
JOURNAL OF NATURAL PRODUCTS
卷 84, 期 5, 页码 1563-1572出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jnatprod.1c00083
关键词
-
资金
- National Center for Research Resources (NCRR), National Institutes of Health (NIH) [P20GM103430]
The study found that CBD exerts protective effects in human keratinocytes by modulating the caspase-1-IL-1 beta axis, supporting its potential applications in promoting skin health.
Preclinical and clinical studies support cannabidiol (CBD)'s antioxidant and anti-inflammatory effects, which are linked to its skin protective effects, but there have been limited mechanistic studies reported. Herein we evaluated CBD's protective effects against hydrogen peroxide (H2O2)-induced oxidative stress in human keratinocyte HaCaT cells and explored its possible mechanism(s) of action. CBD (10 mu M) protected HaCaT cells by alleviating H2O2 (200 mu M)-induced cytotoxicity (by 11.3%) and reactive oxygen species (total- and mitochondrial-derived). Several NLRP3 inflammasome-related genes including CASP1 and IL1B were identified as potential molecular targets for CBD's antioxidant effects by multiplexed gene and network pharmacology analyses. CBD treatment down-regulated the mRNA expression levels of CASP1 and IL1B (by 32.9 and 51.0%, respectively) and reduced IL-1 beta level (by 16.2%) in H2O2-stimulated HaCaT cells. Furthermore, CBD inhibited the activity of caspase-1 enzyme (by 15.7%) via direct binding to caspase-1 protein, which was supported by data from a biophysical binding assay (surface plasmon resonance) and a computational docking experiment. In addition, CBD mitigated H2O2-induced pyroptosis (capase-1-mediated cell death) and apoptosis by 23.6 and 44.0%, respectively. The findings from the current study suggest that CBD exerts protective effects in human keratinocytes via the modulation of the caspase-1-IL-1 beta axis, supporting its potential skin health applications.
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