Abstract
Chenopodium quinoa Wild is a “pseudocereal” grain which attracts a lot of attention in the scientific community as it has a positive effect on health. Here, we investigate the presence of biologically active O-prenylated phenylpropanoids in the ethanol extract of commercially available quinoa seeds. We claim that 4′-Geranyloxyferulic acid (GOFA) was the only phytochemical product found that belongs to quinoa’s group secondary metabolites. We studied the changes in the oxidative and inflammatory status of the cellular environment in HCT 116 cell line processed with quinoa extract and its component GOFA; the implementation was done through the analysis of the antioxidant enzymes (SOD and CAT), the pro-inflammatory components (iNOS, IL-6 and TNF-α), and the products of intermediary metabolism (ONOO−, O2−). Moreover, the l-arginine uptake was proposed as a target of the tested compounds. We demonstrated that the GOFA, through a decrease of the CAT-2B expression, leads to a reduction of the l-arginine uptake, downregulating the harmful iNOS and restoring the altered redox state. These results propose a new molecular target involved in the reduction of the critical inflammatory process responsible for the cancer progression.
Highlights
The control of colorectal cancer (CRC) can be implemented by the potential of alternative therapies
We have demonstrated that Amaranthus retroflexus L. belongs to the Amaranthaceae family and contains the oxyprenylated phenylpropanoids, a rare class of biologically active natural products as 7-isopentenyloxycoumarin, auraptene, umbelliprenin, and 4 -geranyloxyferulic acid (GOFA) [15]
As C. quinoa belongs to the same taxonomic family we investigated the presence of oxyprenylated phenylpropanoids in the ethanol extract of C. quinoa seeds using commercially available roasted seeds
Summary
The control of colorectal cancer (CRC) can be implemented by the potential of alternative therapies. In the past few years, plant extracts, which have anti-inflammatory, antioxidant, anti-proliferative, and anti-angiogenic properties, and are able to block, reverse, or prevent tumor growth, have been used as anticancer therapy [1]. Chronic inflammation, accompanied by an imbalance of the cellular redox state, has been implicated as a potential biological mechanism in the progression of colorectal cancer in humans. This condition leads to the release of inflammatory cytokines and chemokines which promote proliferation, angiogenesis, invasion, and metastasis, and facilitate tumor growth [3]. The phlogistic mediators NO, and the pro-inflammatory cytokine TNF-alpha, can be considered as key mediators of inflammatory processes which activate angiogenic processes and determine the synthesis of different chemokines in the colonic mucosa of CRC patients [5,6]
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