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Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health. Recent studies suggest that fine particulate matter of less than 2.5 (PM2.5), common in air pollution, can reach the brain, potentially resulting in the development and acceleration of various neurological disorders including Alzheimer’s disease, Parkinson’s disease, and other forms of dementia, but the underlying pathological mechanisms are not clear. Astaxanthin is a red-colored phytonutrient carotenoid that has been known for anti-inflammatory and neuroprotective effects. In this study, we demonstrated that exposure to PM2.5 increases the neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia (DAM) signature markers in microglial cells, and that treatment with astaxanthin can prevent the neurotoxic effects of this exposure through anti-inflammatory properties. Diesel particulate matter (Sigma-Aldrich) was used as a fine particulate matter 2.5 in the present study. Cultured rat glial cells and BV-2 microglial cells were treated with various concentrations of PM2.5, and then the expression of various inflammatory mediators and signaling pathways were measured using qRT-PCR and Western blot. Astaxanthin was then added and assayed as above to evaluate its effects on microglial changes, inflammation, and toxicity induced by PM2.5. PM2.5 increased the production of nitric oxide and reactive oxygen species and upregulated the transcription of various proinflammatory markers including Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor α (TNFα), inducible nitric oxide synthase (iNOS), triggering receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor 2/4 (TLR2/4), and cyclooxygenase-2 (COX-2) in BV-2 microglial cells. However, the mRNA expression of IL-10 and arginase-1 decreased following PM2.5 treatment. PM2.5 treatment increased c-Jun N-terminal kinases (JNK) phosphorylation and decreased Akt phosphorylation. Astaxanthin attenuated these PM2.5-induced responses, reducing transcription of the proinflammatory markers iNOS and heme oxygenase-1 (HO-1), which prevented neuronal cell death. Our results indicate that PM2.5 exposure reformulates microglia via proinflammatory M1 and DAM phenotype, leading to neurotoxicity, and the fact that astaxanthin treatment can prevent neurotoxicity by inhibiting transition to the proinflammatory M1 and DAM phenotypes. These results demonstrate that PM2.5 exposure can induce brain damage through the change of proinflammatory M1 and DAM signatures in the microglial cells, as well as the fact that astaxanthin can have a potential beneficial effect on PM2.5 exposure of the brain.
Air pollution has become one of the most serious issues for human health and has been shown to be particularly concerning for neural and cognitive health. Recent studies suggest that fine particulate matter of less than 2.5 (PM2.5), common in air pollution, can reach the brain, potentially resulting in the development and acceleration of various neurological disorders including Alzheimer’s disease, Parkinson’s disease, and other forms of dementia, but the underlying pathological mechanisms are not clear. Astaxanthin is a red-colored phytonutrient carotenoid that has been known for anti-inflammatory and neuroprotective effects. In this study, we demonstrated that exposure to PM2.5 increases the neuroinflammation, the expression of proinflammatory M1, and disease-associated microglia (DAM) signature markers in microglial cells, and that treatment with astaxanthin can prevent the neurotoxic effects of this exposure through anti-inflammatory properties. Diesel particulate matter (Sigma-Aldrich) was used as a fine particulate matter 2.5 in the present study. Cultured rat glial cells and BV-2 microglial cells were treated with various concentrations of PM2.5, and then the expression of various inflammatory mediators and signaling pathways were measured using qRT-PCR and Western blot. Astaxanthin was then added and assayed as above to evaluate its effects on microglial changes, inflammation, and toxicity induced by PM2.5. PM2.5 increased the production of nitric oxide and reactive oxygen species and upregulated the transcription of various proinflammatory markers including Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Tumor necrosis factor α (TNFα), inducible nitric oxide synthase (iNOS), triggering receptor expressed on myeloid cells 2 (TREM2), Toll-like receptor 2/4 (TLR2/4), and cyclooxygenase-2 (COX-2) in BV-2 microglial cells. However, the mRNA expression of IL-10 and arginase-1 decreased following PM2.5 treatment. PM2.5 treatment increased c-Jun N-terminal kinases (JNK) phosphorylation and decreased Akt phosphorylation. Astaxanthin attenuated these PM2.5-induced responses, reducing transcription of the proinflammatory markers iNOS and heme oxygenase-1 (HO-1), which prevented neuronal cell death. Our results indicate that PM2.5 exposure reformulates microglia via proinflammatory M1 and DAM phenotype, leading to neurotoxicity, and the fact that astaxanthin treatment can prevent neurotoxicity by inhibiting transition to the proinflammatory M1 and DAM phenotypes. These results demonstrate that PM2.5 exposure can induce brain damage through the change of proinflammatory M1 and DAM signatures in the microglial cells, as well as the fact that astaxanthin can have a potential beneficial effect on PM2.5 exposure of the brain.
Astaxanthin is a ketocarotenoid, super antioxidant molecule. It has higher antioxidant activity than a range of carotenoids, thus has applications in cosmetics, aquaculture, nutraceuticals, therapeutics, and pharmaceuticals.Naturally, it is derived from Haematococcus pluvialis via a one-stage process or two-stage process. Natural astaxanthin significantly reduces oxidative and free-radical stress as compared to synthetic astaxanthin. The present review summarizes all the aspects of astaxanthin, including its structure, chemistry, bioavailability, and current production technology. Also, this paper gives a detailed mechanism for the potential role of astaxanthin as nutraceuticals for cardiovascular disease prevention, skin protection, antidiabetic and anticancer, cosmetic ingredient, natural food colorant, and feed supplement in poultry and aquaculture. Astaxanthin is one of the high-valued microalgae products of the future. However, due to some risks involved or not having adequate research in terms of long-term consumption, it is still yet to be explored by food industries. Although the cost of naturally derived astaxanthin is high, it accounts for only a 1% share in total astaxanthin available in the global market. Therefore, scientists are looking for ways to cut down the cost of natural astaxanthin to be made available to consumers.
BACKGROUND Compared with free astaxanthin (Asta), docosahexaenoic acid astaxanthin monoester (Asta‐C22:6) has higher stability and bioavailability. However, Asta‐E is still unable to be used in the water system. Hence it is necessary to build a water‐soluble delivery system. In this study, Asta‐C22:6 microemulsion and microcapsule using whey protein isolate (WPI) and hydroxypropyl‐β‐cyclodextrin (HPβ‐CD) as composite wall material were prepared. They were added to three dairy products (milk powder, yogurt and flavored dairy product). A dairy product rich in Asta‐C22:6 with high bioavailability was designed by measuring quality characteristics, sensory evaluation and in vivo experiments. RESULTS Compared with spray drying, the freeze‐drying microcapsule had a higher encapsulation efficiency (72.5%), water content (4%) and better solubility, and Asta‐C22:6 microcapsule (1 g L−1) yogurt had the best quality. The bioavailability of Asta‐C22:6 microcapsule yogurt was further evaluated. After a single oral dose in mice, the bioavailability of Asta‐C22:6 microcapsule in yogurt was significantly increased (Cmax = 0.31 μg mL−1, AUC0–T = 3.20 h μg mL−1). CONCLUSION We successfully prepared Asta‐C22:6 microcapsule yogurt, which improved the stability and bioavailability of Asta. The present research is meaningful for delivering unstable bioactive small molecules based on WPI and HPβ‐CD. It provides an experimental basis for the application of Asta‐C22:6 and the development of functional dairy products. © 2022 Society of Chemical Industry.
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