PMID: 

Biomacromolecules. 2020 May 18. Epub 2020 May 18. PMID: 32421313

Abstract Title: 

Fucoidan immobilized at the surface of a fibrous mesh presents toxic effects over melanoma cells, but not over non-cancer skin cells.

Abstract: 

The use of fucoidan, a marine-origin bioactive polymer, is herein proposed as a component of an innovative and effective strategy against melanoma, one of the rarest but most aggressive skin cancers. First, fucoidan antitumor activity, in its soluble form, was assessed presenting increased cytotoxicity over melanoma cells, when compared to human dermal fibroblasts and keratinocytes. After this antitumor activity validation and trying to develop a more targeted and local strategy aiming to diminish the cytotoxic effects over non-cancer cells, fucoidan was immobilized at the surface of electrospun nanofibrous mesh (Fu_NFM), envisioning the development of a therapeutic patch. The maximum immobilization concentration was 1.2 mg mL -1, determined by the Toluidine Blue Assay and confirmed by XPS. Furthermore, NFM_Fu is more hydrophilic than NFM, presenting a contact angle of 36º, lower than the 121º of the control condition. NFM_Fu was able to reduce human melanoma cells viability by 50% without affecting human dermal fibroblasts and keratinocytes. Taken together, these results may set the basis for a valuable approach for melanoma treatment.

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PMID: 

Molecules. 2020 May 19 ;25(10). Epub 2020 May 19. PMID: 32438702

Abstract Title: 

Protective Effects of Fucoidan Isolated from Celluclast-Assisted Extract ofSporophylls against AAPH-Induced Oxidative Stress In Vitro and In Vivo Zebrafish Model.

Abstract: 

Fucoidan is a fucose-enriched polysaccharide, obtained from brown algae, with demonstrated antioxidant properties. However, traditional extraction methods using water or chemical-based extraction methods have reduced yield and produced hazardous by-products. In this study, we isolated fucoidan at a high yield using enzyme-assisted extraction; the Celluclast enzyme assisted extract ofsporophylls (FCUS). To examine the antioxidant properties of FCUS, oxidative stress was induced with 2,2'-azobis (2-methylpropionamidine) dihydrochloride (AAPH) in Vero cells and zebrafish model. FCUS was composed of 30.4% sulfate and 52.3% fucose. Pre-treatment of Vero cells with FCUS dose dependently inhibited AAPH-induced reactive oxygen species (ROS) production. Moreover, FCUS remarkably reduced cell death, ROS generation, and lipid peroxidation production in zebrafish larvae. Overall, these findings indicate that the sulfate-rich fucoidan of FCUS, obtained with an eco-friendly process, could be implemented as a beneficial antioxidant agent in the functional food industry.

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Originally published on www.thesacredscience.com

Why do so many people equate relaxation and pleasure with walking barefoot along the beach as the waves roll in? How come my son River’s first instinct is to take his shoes off when he sees a field of green grass?

Is it kooky human behavior that is simply hard-wired into our genetic makeup, or is there something more to this urge to remove footwear?

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PMID: 

Food Funct. 2020 Apr 30 ;11(4):3361-3370. PMID: 32232236

Abstract Title: 

Fucoxanthin alleviates palmitate-induced inflammation in RAW 264.7 cells through improving lipid metabolism and attenuating mitochondrial dysfunction.

Abstract: 

In this study, we aimed to examine the effects of fucoxanthin on inflammation triggered by palmitate in macrophages. Raw 264.7 cells were treated with palmitate with or without fucoxanthin co-treatment. Fucoxanthin greatly alleviated palmitate-induced decrease in cell viability and loss of mitochondrial membrane potential. Fucoxanthin also significantly attenuated the palmitate-induced transcriptional expression of Il-6, Il-1β, Tnfα and Nlrp3 inflammasomes and increased the expression of Tgfb. In addition, fucoxanthin decreased triglyceride accumulation induced by palmitate through enhancing the expression of Cpt1a, Pparg and other lipid metabolism genes. Inhibition of CPT1a by etomoxir attenuated the anti-inflammatory effect of fucoxanthin. Furthermore, fucoxanthin increased AMPK phosphorylation and AMPKa1 knockdown by its specific siRNA diminished protective function. In addition, fucoxanthin restored palmitate-mediated mitochondrial dysfunction and improved mitophagy-related gene expression. These findings suggest that fucoxanthin could attenuate free fatty acid-induced inflammation in macrophages through modulating lipid metabolism and mitigating mitochondrial dysfunction.

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PMID: 

Int J Mol Sci. 2020 Mar 22 ;21(6). Epub 2020 Mar 22. PMID: 32235696

Abstract Title: 

Fucoxanthin Ameliorates Atopic Dermatitis Symptoms by Regulating Keratinocytes and Regulatory Innate Lymphoid Cells.

Abstract: 

Fucoxanthin (FX) is a xanthophyll that is contained abundantly in marine plants. The biological action of FX includes its antioxidant and anti-lipogenic activities, while the precise action of its mechanisms on skin cells has not yet been clarified. The current study examined the effect of FX in comparison with tacrolimus (TAC) on NC/Nga mice, which are an atopic dermatitis (AD) model. FX topical treatment dramatically ameliorated itching behavior over the TAC treatment, which was insufficient for improvement of AD symptoms. In Nc/Nga mice, FX or TAC applied to the skin inhibited eosinophil infiltration with decreased expression of Il-33. FX also stimulated Il-2, Il-5, Il-13, Il-10, and TGF-β expression levels, and Sca1Il-10TGF-βregulatory innate lymphoid cells (ILCreg) were dominantly observed in FX treated skin epidermal keratinocytes and dermal layers. This combined evidence demonstrated that FX exerts anti-inflammatory effects on keratinocytes and ameliorates AD symptoms by regulating ILCreg to normalize immune responses in an atopic dermatitis model.

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PMID: 

J Physiol Pharmacol. 2020 Feb ;71(1). Epub 2020 Apr 27. PMID: 32350150

Abstract Title: 

Spent hops (Humulus Lupulus L.) extract as modulator of the inflammatory response in lipopolysaccharide stimulated RAW 264.7 macrophages.

Abstract: 

Macrophages play important roles in acute and chronic inflammation. Upon their activation, they secrete a variety of mediators, including eicosanoids, nitric oxide and cytokines, which play different roles in the stimulation and resolution of inflammatory processes. There is a continuous search for selective modulators of these processes. Natural polyphenols and polyphenol-rich extracts have been found to possess preventive and therapeutic potential, including by their anti-inflammatory effects. In this study, the inhibition of the formation of inflammatory mediators by the spent hops extract (SHE), a polyphenol-rich extract from Humulus Lupulus L., was examined using lipopolysaccharide (LPS)- activated murine macrophages (RAW 264.7). The SHE suppressed inter alia the interleukin-6 (IL-6) mRNA expression to 32% in LPS-activated macrophages and to 61% at a protein level (at 25μg/mL). SHE reduced both the cyclooxygenase-2 (COX-2) mRNA expression to 47% and their protein expression to 32%. Not only did SHE inhibit the IL-6 and COX-2 levels but also decreased both inducible nitric oxide synthase (iNOS) protein expression to 2% at 25 μg/mL and nitric oxide (NO) productionfor all tested concentrations. The inhibited expression of these inflammatory molecules was likely caused by the reduced activity of nuclear factor-κB (NF-κB). Both mRNA and protein expression of NF-κB was decreased to 38% and 42%, respectively. These results provide the first evidence that SHE decreases the expression of proinflammatory cytokines and inflammatory mediators, which merits further studies to investigate the potential of SHE as anti-inflammatory preparation.

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PMID: 

Chem Biol Interact. 2020 Jun 1 ;324:109095. Epub 2020 Apr 11. PMID: 32289289

Abstract Title: 

Anti-rheumatic activity of Phenethyl isothiocyanate via inhibition of histone deacetylase-1.

Abstract: 

Rheumatoid Arthritis (RA) affects approximately 1% of the total world population. Despite incessant research and development of new therapeutic agents, management of RA is still a troublesome affair. Histone Deacetylase 1 (HDAC1) is an epigenetic regulator which play important role in pathogenesis of RA. In present study, we hypothesized that Phenethyl isothiocyanate (PEITC), a potent inhibitor of HDAC1, may ameliorate RA. Efficacy of PEITC was evaluated in Complete Freund's Adjuvant (CFA) induced arthritis model in rats. CFA (0.1 ml) was injected subplantarly in the left hind paw on day 0 to all the groups except normal control. The administration of test drug PEITC (10, 24&50 mg/kg) and standard drug Ibuprofen started simultaneously and was continued for 21 days. Paw edema, total arthritic index, mobility score, stair climbing ability, behavioral parameters, and bone erosion were evaluated. Further, radiographic studies, TNF-alpha as well as HDAC1 levels in synovial tissue homogenate and histological analysis were performed. Prophylactic treatment of PEITC attenuated paw edema, total arthritic index, mobility score, stair climbing ability, behavioral parameters, and bone erosion in dose dependent manner. Furthermore, there was significant decrease in TNF-alpha aswell as HDAC1 levels in synovial tissue homogenate. Histological analysis revealed no cartilage damage, bone erosion, hyperplasia at synovial lining as well as infiltration of inflammatory cells in treatment group. Results of this study suggest potent anti-rheumatoid arthritis activity of Phenethylisothiocyanate in CFA induced RA model in rats.

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PMID: 

Oxid Med Cell Longev. 2020 ;2020:5021983. Epub 2020 Apr 4. PMID: 32322335

Abstract Title: 

-Phenethyl Isothiocyanate Induces Cell Death in Human Osteosarcoma through Altering Iron Metabolism, Disturbing the Redox Balance, and Activating the MAPK Signaling Pathway.

Abstract: 

Osteosarcoma is the most common primary malignancy of the skeleton in children and adults. The outcomes of people with osteosarcomas are unsatisfied.-Phenethyl isothiocyanate (PEITC) exhibits chemoprevention and chemotherapeutic activities against many human cancers. The molecular mechanism underlying its action on osteosarcoma is still unknown. This study was aimed at investigating the effect of PEITC on human osteosarcoma bothand. The results showed that PEITC reduced cell viability, inhibited proliferation, and caused G/M cell cycle arrest in four human osteosarcoma cell lines (MNNG/HOS, U-2 OS, MG-63, and 143B). Then, we found that PEITC altered iron metabolism related to the processes of iron import, storage, and export, which resulted in increased labile iron. Expectedly, PEITC caused oxidative stress as a consequence of GSH depletion-inducing ROS generation and lipid peroxidation. Multiple cell death modalities, including ferroptosis, apoptosis, and autophagy, were triggered in human osteosarcoma cells. Three MAPKs (ERK, p38, and JNK) were all activated after PEITC treatment; however, they presented different responses among the four human osteosarcoma cell lines. ROS generation was proved to be the major cause of PEITC-induced decreased proliferative potential, altered iron metabolism, cell death, and activated MAPKs in human osteosarcoma cells. In addition, PEITC also significantly delayed tumor growth in a xenograft osteosarcoma mouse model with a 30 mg/kg administration dose. In conclusion, this study reveals that PEITC simultaneously triggers ferroptosis, apoptosis, and autophagy in human osteosarcoma cells by inducing oxidative stress.

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PMID: 

Mol Biol Rep. 2020 Apr ;47(4):2417-2425. Epub 2020 Feb 27. PMID: 32108303

Abstract Title: 

Xanthohumol protects neuron from cerebral ischemia injury in experimental stroke.

Abstract: 

Treatment of antioxidants is necessary to protect ischemic stroke associated neuronal damage. Xanthohumol (XN), a natural flavonoid extracted from hops, has been reported to have potential function as an antioxidant and can be used for neuro protection. However, the role of XN in ischemic stroke remains unclear. Here, we studied the neuroprotective effects of XN through experimental stroke models. Middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation (OGD) was used as in vivo and in vitro model, respectively. We found that the treatment of XN improved MCAO-induced brain injury by reducing infarct size, improving neurological deficits, reversing neuronal damage, reducing oxidative stress injury and cell apoptosis. Further experimental studies showed that XN could revive neuronal apoptosis induced by OGD by preventing oxidative stress injury. In addition, our study suggested that these effects were related to the inhibition of phosphorylation of p38-MAPK and the mediation of nuclear Nrf2 activation. In conclusion, the neuroprotective effects of XN showed in this study make XN a promising supplement for ischemic stroke protection.

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PMID: 

Cells. 2020 Apr 10 ;9(4). Epub 2020 Apr 10. PMID: 32290112

Abstract Title: 

Xanthohumol, a Prenylated Flavonoid from Hops, Induces DNA Damages in Colorectal Cancer Cells and Sensitizes SW480 Cells to the SN38 Chemotherapeutic Agent.

Abstract: 

In spite of chemotherapy and systematic screening for people at risk, the mortality rate of colorectal cancer (CRC) remains consistently high, with 600,000 deaths per year. This low success rate in the treatment of CRC results from many failures associated with high resistance and the risk of metastasis. Therefore, in response to these therapeutic failures, new strategies have been under development for several years aimed at increasing the effect of anticancer compounds and/or at reducing their secondary effects on normal cells, thus enabling the host to better withstand chemotherapy. This study highlights that xanthohumol (Xn) concentrations under the ICvalues were able to induce apoptosis and to enhance the DNA-damage response (DDR). We demonstrate for the first time that Xn exerts its anticancer activity in models of colon cancer through activation of the ataxia telangiectasia mutated (ATM) pathway. Subsequently, the ability of Xn to restore DNA damage in CRC cells can sensitize them to anticancer agents such as SN38 (7-ethyl-10-hydroxycamptothecin) used in chemotherapy.

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