Microalgae offer a sustainable and versatile source of bioactive compounds. Their rapid growth, efficient CO2 utilization, and adaptability make them a promising alternative to traditional production methods. Key compounds, such as proteins, polyunsaturated fatty acids (PUFAs), polyphenols, phytosterols, pigments, and mycosporine-like amino acids (MAAs), hold significant commercial value and are widely utilized in food, nutraceuticals, cosmetics, and pharmaceuticals, driving innovation across multiple industries. Their antiviral and enzyme-producing capabilities further enhance industrial and medical applications. Additionally, microalgae-based biostimulants and plant elicitor peptides (PEPs) contribute to sustainable agriculture by enhancing plant growth and resilience to environmental stressors. The GRAS status of several species facilitates market integration, but challenges in scaling and cost reduction remain. Advances in biotechnology and metabolic engineering will optimize production, driving growth in the global microalgae industry. With increasing consumer demand for natural, eco-friendly products, microalgae will play a vital role in health, food security, and environmental sustainability.
NANOG is a key transcription factor required for maintaining pluripotency of embryonic stem cells. Elevated NANOG expression levels have been reported in many types of human cancers, including lung, oral, prostate, stomach, breast, and brain. Several studies reported the correlation between NANOG expression and tumor metastasis, revealing itself as a powerful biomarker of poor prognosis. However, how NANOG regulates tumor progression is still not known. We previously showed in medaka fish that Nanog regulates primordial germ cell migration through Cxcr4b, a chemokine receptor known for its ability to promote migration and metastasis in human cancers. Therefore, we investigated the role of human NANOG in CXCR4-mediated cancer cell migration. Of note, we found that NANOG regulatory elements in the CXCR4 promoter are functionally conserved in medaka fish and humans, suggesting an evolutionary conserved regulatory axis. Moreover, CXCR4 expression requires NANOG in human glioblastoma cells. In addition, transwell assays demonstrated that NANOG regulates cancer cell migration through the SDF1/CXCR4 pathway. Altogether, our results uncover NANOG-CXCR4 as a novel pathway controlling cellular migration and support Nanog as a potential therapeutic target in the treatment of Nanog-dependent tumor progression.
Oxidative stress (OS) can induce cell apoptosis and thus plays an important role in aging. Antioxidant foods protect tissues from OS and contribute to a healthier lifestyle. In this study, we described the used of medaka embryos ( Oryzias latipes ) to study the putative antioxidant capacity of dietary cocoa extract in vertebrates. A polyphenol-enriched cocoa extract regulated the expression of several genes implicated in OS, thereby protecting fish embryos from induced OS. The cocoa extract activated superoxide dismutase enzyme activity in embryos and adult fish tissues, suggesting a common mechanism for protection during embryonic development and adulthood. Furthermore, long-term feeding of the cocoa extract increased fish life span. Our study demonstrates that the polyphenol-enriched cocoa extract decreases OS and extends life span in medaka fish, validating the use of medaka embryos as an economical platform to screen the antioxidant capacity of food compounds.
In the present study, selected cosmeceutical properties of aqueous extracts from the microalgae strain Trachydiscus minutus were assessed and compared with those obtained using three widely used Chlorella strains (C. vulgaris, C. sorokiniana, and C. minutissima). Among all extracts, T. minutus extracts showed the highest total antioxidant capacity (TAC) and inhibitory potency towards elastase, suggesting potential activity in controlling skin aging. Furthermore, the cytotoxicity, anti-inflammatory activity and UVA protection of T. minutus extract were evaluated employing normal human dermal fibroblasts (NHDF) and human keratinocyte HaCaT cells. The results showed that the T. minutus extract was able to significantly inhibit the transcription of selected marker genes involved in inflammation [interleukin-6 (IL-6), interleukin-8 (IL-8) and tumor necrosis factor alpha (TNFα)]. In addition, treatment of NHDF and HaCaT cells with T. minutus extract ameliorate the UVA-induced cell damage by decreasing the accumulation of reactive oxygen species (ROS). Extracts from T. minutus were formulated into a skin care cream and an aqueous gel. Both formulas exhibited excellent compatibility and stability. Comprehensively, all these results suggest that T. minutus extract displays promising cosmeceutical properties by providing antioxidant, anti-aging, and anti-inflammatory activities, and therefore has potential for cosmeceutical use.
Air pollution is a growing threat to human health. Airborne pollution effects on respiratory, cardiovascular and skin health are well-established. The main mechanisms of air-pollution-induced health effects involve oxidative stress and inflammation. The present study evaluates the potential of a polyphenol-enriched food supplement ingredient comprising Lippia citriodora, Olea europaea, Rosmarinus officinalis, and Sophora japonica extracts in mitigating the adverse effects of environmental pollution on skin and cardiopulmonary systems. Both in vitro and ex vivo studies were used to assess the blend’s effects against pollution-induced damage. In these studies, the botanical blend was found to reduce lipid peroxidation, inflammation (by reducing IL-1α), and metabolic alterations (by regulating MT-1H, AhR, and Nrf2 expression) in human skin explants exposed to a mixture of pollutants. Similar results were also observed in keratinocytes exposed to urban dust. Moreover, the ingredient significantly reduced pollutant-induced ROS production in human endothelial cells and lung fibroblasts, while downregulating the expression of apoptotic genes (bcl-2 and bax) in lung fibroblasts. Additionally, the blend counteracted the effect of urban dust on the heart rate in zebrafish embryos. These results support the potential use of this supplement as an adjuvant method to reduce the impact of environmental pollution on the skin, lungs, and cardiovascular tissues.
Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder, of the so-called minority diseases, due to its low prevalence. It is caused by an abnormally long track of glutamines (polyQs) in mutant huntingtin (mHtt), which makes the protein toxic and prone to aggregation. Many pathways of clearance of badly-folded proteins are disrupted in neurons of patients with HD. In this work, we show that one Mn(II) quinone complex (4QMn), designed to work as an artificial superoxide dismutase, is able to activate both the ubiquitin-proteasome system and the autophagy pathway in vitro and in vivo models of HD. Activation of these pathways degrades mHtt and other protein-containing polyQs, which restores proteostasis in these models. Hence, we propose 4QMn as a potential drug to develop a therapy to treat HD.