Fucoxanthin Enhances the Level of Reduced Glutathione via the Nrf2-Mediated Pathway in Human Keratinocytes

Zheng, Jian; Piao, Mei Jing; Kim, Ki Cheon; Yao, Cheng Wen; Won, Ji; Hyun, Jin Won

doi:10.3390/md12074214

Cited by 46 publications

(42 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Moreover, PI3K inhibitors significantly abolished the neuroprotective effects of fucoxanthin. These results suggested that fucoxanthin produced neuroprotective effects at least partially via the activation of the prosurvival PI3K/Akt pathway, which is consistence with a report that fucoxanthin activated the PI3K/Akt cascade to decrease cell injury [ 31 ]. Moreover, fucoxanthin attenuated A β oligomer-induced increase of pERK in SH-SY5Y cells, indicating that the inhibition of proapoptotic ERK pathway participated in the neuroprotective effects of fucoxanthin.…”

Section: Discussionsupporting

confidence: 88%

Fucoxanthin, a Marine Carotenoid, Attenuates β‐Amyloid Oligomer‐Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH‐SY5Y Cells

Lin

Zhao

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Alzheimer's disease (AD), the most common neurodegenerative disorder, is characterized by neurofibrillary tangles, synaptic impairments, and loss of neurons. Oligomers of β-amyloid (Aβ) are widely accepted as the main neurotoxins to induce oxidative stress and neuronal loss in AD. In this study, we discovered that fucoxanthin, a marine carotenoid with antioxidative stress properties, concentration dependently prevented Aβ oligomer-induced increase of neuronal apoptosis and intracellular reactive oxygen species in SH-SY5Y cells. Aβ oligomers inhibited the prosurvival phosphoinositide 3-kinase (PI3K)/Akt cascade and activated the proapoptotic extracellular signal-regulated kinase (ERK) pathway. Moreover, inhibitors of glycogen synthase kinase 3β (GSK3β) and mitogen-activated protein kinase (MEK) synergistically prevented Aβ oligomer-induced neuronal death, suggesting that the PI3K/Akt and ERK pathways might be involved in Aβ oligomer-induced neurotoxicity. Pretreatment with fucoxanthin significantly prevented Aβ oligomer-induced alteration of the PI3K/Akt and ERK pathways. Furthermore, LY294002 and wortmannin, two PI3K inhibitors, abolished the neuroprotective effects of fucoxanthin against Aβ oligomer-induced neurotoxicity. These results suggested that fucoxanthin might prevent Aβ oligomer-induced neuronal loss and oxidative stress via the activation of the PI3K/Akt cascade as well as inhibition of the ERK pathway, indicating that further studies of fucoxanthin and related compounds might lead to a useful treatment of AD.

show abstract

Section: Discussionsupporting

confidence: 88%

Fucoxanthin, a Marine Carotenoid, Attenuates β‐Amyloid Oligomer‐Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH‐SY5Y Cells

Lin

Zhao

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Biochemical experiments indicated that knockdown of NRF2 could increase MDA concentration and decrease concentration of SOD, GSH and CAT, enhancing the effects of laminarin in MRC-5 cells. Numerous studies have proved the protective role of NRF2 against oxidation in various cell types, keratinocytes ( Madduma Hewage et al, 2016 ; Zheng et al, 2014 ), pancreatic β-cells ( Dinić et al, 2016 ), mesenchymal stem cells ( Loseva et al, 2012 ), amongst others, elevating SOD, GSH and CAT cellular concentration. Besides, up-regulation of NRF2 was accompanied with suppressed MDA level during the amelioration of oxidative damage ( Xie et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

Lü

Liu

Zhai

et al. 2017

PeerJ

View full text Add to dashboard Cite

Oxidative damage is a major cause of lung diseases, including pulmonary fibrosis. Laminarin is a kind of polysaccharide extracted from brown algae and plays vital roles in various biological processes. However, the functions and mechanisms of laminarin in pulmonary oxidative damage are poorly understood. This study aimed at investigating the protective effect of laminarin against pulmonary oxidative damage and underlying mechanisms. Human lung fibroblasts MRC-5 cells were treated with hydrogen peroxide to induce oxidative damage. Laminarin treatment was performed before or after hydrogen peroxide treatment, and then major indexes of oxidative damage, including superoxide dismutase (SOD), malondialdehyde (MDA), reduced glutathione (GSH) and catalase (CAT), were quantified by biochemical assays. The expression of oxidation-related factor, nuclear factor erythroid 2 like 2 (NRF2) was analyzed by qPCR, Western blot and immunofluorescence assay. NRF2 knockdown and overexpression were performed by cell transfection to reveal possible mechanisms. Results showed that laminarin treatment of 0.020 mg/mL for 24 h, especially the pre-treatment, could significantly relieve changes in SOD, MDA, GSH and CAT that were altered by hydrogen peroxide, and promote NRF2 mRNA (P < 0.001). NRF2 protein was also elevated by laminarin, and nuclear translocation was observed. Factors in NRF2 signaling pathways, including KEAP1, NQO1, GCLC and HO1, were all regulated by laminarin. Roles of NRF2 were tested, suggesting that NRF2 regulated the concentration of SOD, MDA, GSH and CAT, suppressed KEAP1, and promoted NQO1, GCLC and HO1. These findings suggested the protective role of laminarin against pulmonary oxidative damage, which might involve the regulation of NRF2 signaling pathways. This study provided information for the clinical application of laminarin to pulmonary diseases like pulmonary fibrosis.

show abstract

“…Moreover, the protective effects of fucoxanthin against oxidative damage were related to inhibition of apoptosis through down-regulation of Bax expression and increase of Bcl-2 expression [ 329 ]. More recently, Zheng et al [ 330 ] studied the antioxidant activity of fucoxanthin in HaCaT cells and showed that this treatment increased the expression of glutamate-cysteine ligase catalytic subunit (GCLC) and glutathione synthetase (GSS), two enzymes involved in reduced glutathione (GSH) synthesis. The mechanisms underlying these effects were related to activation of the transcription factor Nrf2 via PI3K/Akt, which in turn activated the transcription of ARE-driven GCLC and GSS genes, leading the synthesis of antioxidant GSH.…”

Section: Inflammation and Skin Cancermentioning

confidence: 99%

Bioactive Compounds Isolated from Microalgae in Chronic Inflammation and Cancer

et al. 2015

View full text Add to dashboard Cite

The risk of onset of cancer is influenced by poorly controlled chronic inflammatory processes. Inflammatory diseases related to cancer development include inflammatory bowel disease, which can lead to colon cancer, or actinic keratosis, associated with chronic exposure to ultraviolet light, which can progress to squamous cell carcinoma. Chronic inflammatory states expose these patients to a number of signals with tumorigenic effects, including nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPK) activation, pro-inflammatory cytokines and prostaglandins release and ROS production. In addition, the participation of inflammasomes, autophagy and sirtuins has been demonstrated in pathological processes such as inflammation and cancer. Chemoprevention consists in the use of drugs, vitamins, or nutritional supplements to reduce the risk of developing or having a recurrence of cancer. Numerous in vitro and animal studies have established the potential colon and skin cancer chemopreventive properties of substances from marine environment, including microalgae species and their products (carotenoids, fatty acids, glycolipids, polysaccharides and proteins). This review summarizes the main mechanisms of actions of these compounds in the chemoprevention of these cancers. These actions include suppression of cell proliferation, induction of apoptosis, stimulation of antimetastatic and antiangiogenic responses and increased antioxidant and anti-inflammatory activity.

show abstract

Fucoxanthin Enhances the Level of Reduced Glutathione via the Nrf2-Mediated Pathway in Human Keratinocytes

Cited by 46 publications

References 37 publications

Fucoxanthin, a Marine Carotenoid, Attenuates β‐Amyloid Oligomer‐Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH‐SY5Y Cells

Fucoxanthin, a Marine Carotenoid, Attenuates β‐Amyloid Oligomer‐Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH‐SY5Y Cells

Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

Bioactive Compounds Isolated from Microalgae in Chronic Inflammation and Cancer

Contact Info

Product

Resources

About