scholarly journals Antioxidative effects of the spice cardamom against non-melanoma skin cancer by modulating nuclear factor erythroid-2-related factor 2 and NF-κB signalling pathways

2011 ◽  
Vol 108 (6) ◽  
pp. 984-997 ◽  
Author(s):  
Ila Das ◽  
Asha Acharya ◽  
Deborah L. Berry ◽  
Supti Sen ◽  
Elizabeth Williams ◽  
...  

The role of dietary factors in inhibiting or delaying the development of non-melanoma skin cancer (NMSC) has been investigated for many years. Cardamom, which is a dietary phytoproduct, has been commonly used in cuisines for flavour and has numerous health benefits, such as improving digestion and stimulating metabolism and having antitumorigenic effects. We have investigated the efficacy of dietary cardamom against 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin papillomatogenesis in Swiss albino mice that closely resembles human NMSC. Mice were grouped into normal wild type (untreated), vehicle-treated (acetone), carcinogen-treated (DMBA), and DMBA and cardamom-treated (DMBA+CARD) to delineate the role of cardamom against DMBA-induced papillomatogenesis. Oral administration of cardamom to DMBA-treated mice up-regulated the phase II detoxification enzymes, such as glutathione-S-transferase and glutathione peroxidase, probably via activation of nuclear factor erythroid-2-related factor 2 transcription factor in ‘DMBA+CARD’ mice. Furthermore, reduced glutathione, glutathione reductase, superoxide dismutase and catalase were also up-regulated by cardamom in the same ‘DMBA+CARD’ group of mice compared with DMBA-treated mice. Cardamom ingestion in DMBA-treated mice blocked NF-κB activation and down-regulated cyclo-oxygenase-2 expression. As a consequence, both the size and the number of skin papillomas generated on the skin due to the DMBA treatment were reduced in the ‘DMBA+CARD’ group. Thus, the results from the present study suggest that cardamom has a potential to become a pivotal chemopreventive agent to prevent papillomagenesis on the skin.

2019 ◽  
Vol 31 (11) ◽  
pp. 759-768 ◽  
Author(s):  
C. Conforti ◽  
P. Corneli ◽  
C. Harwood ◽  
I. Zalaudek

1997 ◽  
pp. 748-758
Author(s):  
C. A. Harwood ◽  
J. Breuer ◽  
J. M. McGregor ◽  
C. M. Proby ◽  
A. Storey ◽  
...  

2019 ◽  
Vol 10 (3) ◽  
pp. 514-517 ◽  
Author(s):  
Valentina Lancellotta ◽  
Gyoergy Kovács ◽  
Luca Tagliaferri ◽  
Elisabetta Perrucci ◽  
Agata Rembielak ◽  
...  

2018 ◽  
Vol 73 (5) ◽  
pp. 306-313
Author(s):  
Marianna B. Zhilova ◽  
Maria M. Butareva

The review presents modern data on the role of ultraviolet (UV) radiation in the pathogenesis of non-melanoma skin cancer (NMSC), the problem of THE risk of developing NMSC, in particular, squamous cell and basal cell skin cancer both in the population and in long-term repeated irradiation of phototherapy (PUVA therapy, UVB therapy, UVB-311 therapy) in patients with psoriasis. The paper considers the mechanisms of UV-induced cell damage by different spectral ranges (UVA, UVB) including the formation of photoproducts, damage to genomic DNA and other cellular structures, violation of the regulation of signaling pathways, the development of chronic inflammation, secondary immunosuppression. The review summarizes the results of large epidemiological studies discussing the role of gene polymorphisms in the homologous DNA repair XRCC3, gene telomerase TERT-CLPTMI, cytokine IL10 gene, MTHFR gene, encoding the folate synthesis, genes involved in pigmentirovanie MC1R, EXOC2, UBAC2 in the modulation of risk of carcinogenic effect of UV radiation. According to the authors’ opinion, the most vital and significant is data on the role of vitamin D receptor (VDR) gene polymorphisms as possible predictors of the risk of NMSC development. The further prospects of academic research on the cumulative role of the genome and environmental factors in the risk assessment of NMSC are revealed.


2019 ◽  
Vol 60 (4) ◽  
pp. 265-272 ◽  
Author(s):  
Kieran B Garbutcheon‐Singh ◽  
Michael J Veness

2018 ◽  
Vol 19 (10) ◽  
pp. 3109 ◽  
Author(s):  
Eric Romer ◽  
Anita Thyagarajan ◽  
Smita Krishnamurthy ◽  
Christine Rapp ◽  
Langni Liu ◽  
...  

Platelet-activating factor-receptor (PAF-R) agonists are pleiotropic lipid factors that influence multiple biological processes, including the induction and resolution of inflammation as well as immunosuppression. PAF-R agonists have been shown to modulate tumorigenesis and/or tumor growth in various skin cancer models by suppressing either cutaneous inflammation and/or anti-tumoral adaptive immunity. We have previously shown that a chronic systemic PAF-R agonist administration of mice enhances the growth of subcutaneously implanted melanoma tumors. Conversely, chronic topical applications of a PAF-R agonist suppressed non-melanoma skin cancer (NMSC) in a topical chemical carcinogenesis model (dimethylbenz[a]anthracene/phorbol 12-myristate 13-acetate (DMBA/PMA)) in-part via anti-inflammatory effects. These results indicate that the context of PAF-R agonist exposure via either chronic cutaneous or systemic administration, result in seemingly disparate effects on tumor promotion. To further dissect the contextual role of PAF-R agonism on tumorigenesis, we chronically administered systemic PAF-R agonist, carbamoyl-PAF (CPAF) to mice under a cutaneous chemical carcinogenesis protocol, recently characterized to initiate both NMSC and melanocytic nevus formation that can progress to malignant melanoma. Our results showed that while systemic CPAF did not modulate melanocytic nevus formation, it enhanced the growth of NMSC tumors.


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