Anti-proliferative Effects of the Isothiocyanate Sulforaphane on the Growth of Human Cervical Carcinoma HeLa Cells

박성영,; 배송자,; 최영현,

doi:10.5352/jls.2005.15.3.397

Cited by 1 publication

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References 17 publications

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“…Given that glucoraphanin conversion markedly varies (metabolite excretion was 1%-45% of intake) [1], sulforaphane was directly used in the present study. Sulforaphane increases the expression of the p53 gene, which reportedly induces apoptosis in cancer cells, such as liver and cervical cancer cells, maintaining cells in the sub-G1 phase [5]. In autoimmune encephalomyelitis or pulmonary adenoma-induced mice, sulforaphane treatment was shown to exhibit antioxidant effects, decrease the inflammatory response, and suppress the malignant progression of pulmonary adenoma [6,7].…”

Section: Introductionmentioning

confidence: 99%

A Metabolomics Approach to Sulforaphane Efficacy in Secondhand Smoking-Induced Pulmonary Damage in Mice

et al. 2022

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Sulforaphane is an isocyanate abundantly present in cruciferous vegetables. In the present study, we aimed to investigate the effects of sulforaphane on secondhand smoking (SHS)-induced pulmonary damage in mice. Additionally, a metabolomic study was performed to identify biomarkers associated with pulmonary disease using proton nuclear magnetic resonance (1H-NMR) analysis. Male C57BL6J mice were divided into a control group, an SHS exposure group (positive control group, PC), and a sulforaphane treatment group exposed to secondhand smoke (SS) (n = 5 per group). The PC and SS groups were exposed to secondhand smoke in a chamber twice daily for four weeks. Mice in the SS group were orally administered sulforaphane (50 mg/kg) for four weeks during secondhand smoke exposure. Histopathological examination of the lungs revealed pulmonary damage in PC mice, including loss of bronchial epithelial cells, bronchial wall thickening, and infiltration of macrophages. In contrast, mice in the SS group showed little or no epithelial thickening, thereby exhibiting reduced lung damage. Mouse serum and lung tissues were collected and analyzed to determine changes in endogenous metabolites using 1H-NMR. After target profiling, we identified metabolites showing the same tendency in the serum and lung as biomarkers for SHS-induced pulmonary damage, including taurine, glycerol, creatine, arginine, and leucine. As a result of histopathological examination, sulforaphane might inhibit SHS-induced lung damage, and metabolite analysis results suggest potential biomarkers for SHS-induced pulmonary damage in mice.

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