&lt;i&gt;Garcinia vilersiana&lt;/i&gt; bark extract activates the Nrf2/HO-1 signaling pathway in RAW264.7 cells

Shinkai, Yasuhiro; Yamanaka, Ichiro; Duong, Ho Huynh Thuy; Quỳnh, Nguyễn Thị; Kanaho, Yasunori; Kumagai, Yoshito

doi:10.2131/jts.38.875

Cited by 9 publications

(6 citation statements)

References 15 publications

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“…This meant that KC inhibited NO production partly by upregulating the expression of HO-1 in RAW264.7 cells. The Nrf2 is a transcription factor that regulates expression of HO-1 [39]. Further findings demonstrated that Nrf2 was decreased in the cytosols of KC-treated LPS-stimulated RAW 264.7cells, but their DNA-binding activities were concomitantly increased, implying that KC's mediated increase in HO-1 expression was as a result of its action on Nrf2.…”

Section: Discussionmentioning

confidence: 92%

In vitro Anti-Inflammatory and Anti-Oxidative Stress Activities of Kushenol C Isolated from the Roots of Sophora flavescens

Cho¹,

Nchang

Kim

et al. 2020

Molecules

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Kushenol C (KC) is a prenylated flavonoid isolated from the roots of Sophora flavescens aiton. Little is known about its anti-inflammatory and anti-oxidative stress activities. Here, we investigated the anti-inflammatory and anti-oxidative stress effects of KC in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, and tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The results demonstrated that KC dose-dependently suppressed the production of inflammatory mediators, including NO, PGE2, IL-6, IL1β, MCP-1, and IFN-β in LPS-stimulated RAW264.7 macrophages. The study demonstrated that the inhibition of STAT1, STAT6, and NF-κB activations by KC might have been responsible for the inhibition of NO, PGE2, IL-6, IL1β, MCP-1, and IFN-β in the LPS-stimulated RAW264.7 macrophages. KC also upregulated the expression of HO-1 and its activities in the LPS-stimulated RAW264.7 macrophages. The upregulation of Nrf2 transcription activities by KC in the LPS-stimulated RAW264.7 macrophages was demonstrated to be responsible for the upregulation of HO-1 expression and its activity in LPS-stimulated RAW264.7 macrophages. In HaCaT cells, KC prevented DNA damage and cell death by upregulating the endogenous antioxidant defense system involving glutathione, superoxide dismutase, and catalase, which prevented reactive oxygen species production from tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The upregulated activation of Nrf2 and Akt in the PI3K-Akt signaling pathway by KC was demonstrated to be responsible for the anti-oxidative stress activity of KC in HaCaT cells. Collectively, the study suggests that KC can be further investigated as a potential anti-inflammatory candidate for the treatment of inflammatory diseases.

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Section: Discussionmentioning

confidence: 92%

In vitro Anti-Inflammatory and Anti-Oxidative Stress Activities of Kushenol C Isolated from the Roots of Sophora flavescens

Cho¹,

Nchang

Kim

et al. 2020

Molecules

View full text Add to dashboard Cite

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“…The nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates expression of antioxidant and detoxifying genes including heme oxygenase-1 (HO-1). 34) HO-1 plays an important role in the regulation of oxidative stress and inflammatory responses. It is well known that HO-1 is a highly inducible and rate-limiting protein that catalyzes the degradation of heme to carbon monoxide (CO), ferrous iron and biliverdin.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory activity of myricetin from Diospyros lotus through suppression of NF-κB and STAT1 activation and Nrf2-mediated HO-1 induction in lipopolysaccharide-stimulated RAW264.7 macrophages

Cho

Yin²,

Park

et al. 2016

Bioscience, Biotechnology, and Biochemistry

103

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Diospyros lotus is traditionally used for the treatment of diabetes, diarrhea, tumor, and hypertension. The purpose of this study was to investigate the anti-inflammatory effect and underlying molecular mechanisms of myricetin in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Myricetin dose-dependently suppressed the production of pro-inflammatory mediators (NO, iNOS, PGE2, and COX-2) in LPS-stimulated RAW264.7 macrophages. Myricetin administration decreased the production of NO, iNOS, TNF-α, IL-6, and IL-12 in mice. Myricetin decreased NF-κB activation by suppressing the degradation of IκBα, nuclear translocation of p65 subunit of NF-κB, and NF-κB DNA binding activity in LPS-stimulated RAW264.7 macrophages. Moreover, myricetin attenuated the phosphorylation of STAT1 and the production of IFN-β in LPS-stimulated RAW264.7 macrophages. Furthermore, myricetin induced the expression of HO-1 through Nrf2 translocation. In conclusion, these results suggest that myricetin inhibits the production of pro-inflammatory mediators through the suppression of NF-κB and STAT1 activation and induction of Nrf2-mediated HO-1 expression in LPS-stimulated RAW264.7 macrophages.

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“…In contrast, we and others have found little evidence for de novo androgen synthesis in clinical CRPC samples. Moreover, we have previously shown that androgen precursors induced cell growth and AR target gene expression in vitro, but with undetectable CYP17A1‐dependent conversion into testosterone, indicating either direct AR binding or conversion rather than de novo synthesis as a driver of cell growth …”

Section: Introductionmentioning

confidence: 99%

A bypass mechanism of abiraterone‐resistant prostate cancer: Accumulating CYP17A1 substrates activate androgen receptor signaling

et al. 2019

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Background Intratumoral steroidogenesis and its potential relevance in castration‐resistant prostate cancer (CRPC) and in cytochrome P450, family 17, subfamily A, polypeptide 1 (CYP17A1)‐inhibitor treated hormone‐naïve and patients with CRPC are not well established. In this study, we tested if substrates for de novo steroidogenesis accumulating during CYP17A1 inhibition may drive cell growth in relevant preclinical models. Methods PCa cell lines and their respective CRPC sublines were used to model CRPC in vitro. Precursor steroids pregnenolone (Preg) and progesterone (Prog) served as substrate for de novo steroid synthesis. TAK700 (orteronel), abiraterone, and small interfering RNA (siRNA) against CYP17A1 were used to block CYP17A1 enzyme activity. The antiandrogen RD162 was used to assess androgen receptor (AR) involvement. Cell growth was measured by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. AR‐target gene expression was quantified by reverse transcription polymerase chain reaction (RT‐PCR). Nuclear import studies using cells with green fluorescent protein (GFP)‐tagged AR were performed to assess the potential of precursor steroids to directly activate AR. Results Preg and Prog stimulated cell proliferation and AR target gene expression in VCaP, DuCaP, LNCaP, and their respective CRPC sublines. The antiandrogen RD162, but not CYP17A1 inhibition with TAK700, abiraterone or siRNA, was able to block Preg‐ and Prog‐induced proliferation. In contrast to TAK700, abiraterone also affected dihydrotestosterone‐induced cell growth, indicating direct AR binding. Furthermore, Prog‐induced AR translocation was not affected by treatment with TAK700 or abiraterone, while it was effectively blocked by the AR antagonist enzalutamide, further demonstrating the direct AR activation by Prog. Conclusion Activation of the AR by clinically relevant levels of Preg and Prog accumulating in abiraterone‐treated patients may act as a driver for CRPC. These data provide a scientific rationale for combining CYP17A1 inhibitors with antiandrogens, particularly in patients with overexpressed or mutated‐AR.

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<i>Garcinia vilersiana</i> bark extract activates the Nrf2/HO-1 signaling pathway in RAW264.7 cells

Cited by 9 publications

References 15 publications

In vitro Anti-Inflammatory and Anti-Oxidative Stress Activities of Kushenol C Isolated from the Roots of Sophora flavescens

In vitro Anti-Inflammatory and Anti-Oxidative Stress Activities of Kushenol C Isolated from the Roots of Sophora flavescens

Anti-inflammatory activity of myricetin from Diospyros lotus through suppression of NF-κB and STAT1 activation and Nrf2-mediated HO-1 induction in lipopolysaccharide-stimulated RAW264.7 macrophages

A bypass mechanism of abiraterone‐resistant prostate cancer: Accumulating CYP17A1 substrates activate androgen receptor signaling

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