Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

Niu, Tingting; Fu, Gaoqing; Zhou, Jiawei; Han, Hui; Chen, Juanjuan; Wu, Wei; Chen, Haimin

doi:10.3390/md18020105

Cited by 12 publications

(10 citation statements)

References 31 publications

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“…To assess the interference effect of FUC on Nrf2-Keap1 binding, 266 nM Nrf2 and FUC of different concentrations were mixed, and the mixture was used to interact with Keap1 protein. The sensors were loaded with biotinylated Keap1 protein, and the immobilized sensor was dipped into the [18]. Briefly, treated cells were washed once with ice-cold PBS, followed by incubation with 10 μM carboxy-H2DCF-DA at 37°C for 10 min.…”

Section: Fortébio Octet System Assay For Binding Affinity Between Keamentioning

confidence: 99%

Fucoxanthin Prevents 6‐OHDA‐Induced Neurotoxicity by Targeting Keap1

Han

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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As the most abundant marine carotenoid extracted from seaweeds, fucoxanthin (FUC) is considered to have excellent neuroprotective activity. However, the target of FUC for its neuroprotective properties remains largely unclear. Oxidative stress is one of the initiating factors causing neuronal cell loss and necrosis, and it is also an important inducement of Parkinson’s disease (PD). In the present study, the neuroprotective effect of FUC was assessed using a 6-hydroxydopamine- (6-OHDA-) induced neurotoxicity model. FUC suppressed 6-OHDA-induced accumulation of intracellular ROS, the disruption of mitochondrial membrane potential, and cell apoptosis through the Nrf2-ARE pathway. Keap1 as a repressor of Nrf2 can regulate the activity of Nrf2. Here, the biolayer interferometry (BLI) assay demonstrated that FUC specifically targeted Keap1 and inhibited the interaction between Keap1 and Nrf2. FUC bound to the hydrophobic region of Keap1 pocket and formed hydrogen bonding interactions with Arg415 and Tyr525. Besides, it also dose-dependently upregulated the expressions of antioxidant enzymes, such as nicotinamide heme oxygenase-1, glutamate-cysteine ligase modifier subunit, and glutamate-cysteine ligase catalytic subunit, in 6-OHDA-induced PC12 cells. In 6-OHDA-exposed zebrafish, FUC pretreatment significantly increased the total swimming distance of zebrafish larvae and improved the granular region of the brain tissue damage. These results suggested that FUC could protect the neuronal cells against 6-OHDA-induced injury via targeting Keap1.

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Section: Fortébio Octet System Assay For Binding Affinity Between Keamentioning

confidence: 99%

Fucoxanthin Prevents 6‐OHDA‐Induced Neurotoxicity by Targeting Keap1

Han

Liu

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…These findings suggested that HO-1 induction by CoPPIX might contribute to HC protection against gentamicin-induced damage. Recent evidence also suggested that HO-1 was essential in modulating antioxidant effects in other tissues ( Shalaby et al, 2019 ; Niu et al, 2020 ). Park et al (2017) found that in the cochlear tissue, a peroxisome proliferator-activated receptor (PPAR) inducer protected HCs from gentamicin-induced toxicity by increasing the expression of HO-1.…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Protects Hair Cells From Gentamicin-Induced Death

Yang

Chen

Tian

et al. 2022

Front. Cell. Neurosci.

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Gentamicin ototoxicity can generate free radicals within the inner ear, leading to permanent damage to sensory hair cells (HCs) and eventually hearing loss. The following study examined the alterations of oxidative damage-related genes in the cochlea and important molecules responsible for oxidation following gentamicin injury in vitro. The RT2 Profiler polymerase chain reaction (PCR) array was used to screen candidate targets for treatment to prevent hearing loss caused by gentamicin. We found that during gentamicin-induced death in HCs, Heme oxygenase-1 (HO-1) had a high fold change in the HCs of the cochlea. Moreover, the use of CoPPIX to induce HO-1 inhibited gentamicin-induced HC death, while HO-1 inhibitors ZnPPIX after CoPPIX reversed this process. Furthermore, the inhibitors of NF-E2-related factor-2 (Nrf2) reduced the expression of HO-1 and inhibited the protective effect of HO-1 after gentamicin, thus suggesting that the Nrf2/HO-1 axis might regulate gentamicin-associated ototoxicity. We further demonstrated that induction of HO-1 up-regulated the expression of Nrf2 in both cochlear and HEI-OC1 cells. In summary, these findings indicated that HO-1 protects HCs from gentamicin by up-regulating its expression in HCs and interacting with Nrf2 to inhibit reactive oxygen species (ROS).

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“…In addition, Nrf2 also regulate the key genes of heme metabolism ABCB6 , ABCG2 , HO-1 and heme responsive gene-1 to participate in the process of ferroptosis ( Hubner et al, 2009 ; Singh et al, 2010 ; Campbell et al, 2013 ; Dong et al, 2020 ). Among them, HO-1 is not only the key enzyme to decompose heme, but also an important antioxidant ( Tenhunen et al, 1968 ; Niu et al, 2020 ). Multiple studies have shown that activating the antioxidant response axis Nrf2/HO-1 is a crucial means of inhibiting ferroptosis and ameliorating myocardial ischemia-reperfusion injury, ulcerative colitis, and acute lung injury ( Chen et al, 2021b ; Li J. et al, 2021 ; Lv et al, 2021 ).…”

Section: The Regulatory Mechanism Of Ferroptosismentioning

confidence: 99%

Ferroptosis and its role in skeletal muscle diseases

Wang

Zhang

Jiao

et al. 2022

Front. Mol. Biosci.

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Ferroptosis is characterized by the accumulation of iron and lipid peroxidation products, which regulates physiological and pathological processes in numerous organs and tissues. A growing body of research suggests that ferroptosis is a key causative factor in a variety of skeletal muscle diseases, including sarcopenia, rhabdomyolysis, rhabdomyosarcoma, and exhaustive exercise-induced fatigue. However, the relationship between ferroptosis and various skeletal muscle diseases has not been investigated systematically. This review’s objective is to provide a comprehensive summary of the mechanisms and signaling factors that regulate ferroptosis, including lipid peroxidation, iron/heme, amino acid metabolism, and autophagy. In addition, we tease out the role of ferroptosis in the progression of different skeletal muscle diseases and ferroptosis as a potential target for the treatment of multiple skeletal muscle diseases. This review can provide valuable reference for the research on the pathogenesis of skeletal muscle diseases, as well as for clinical prevention and treatment.

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Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

Cited by 12 publications

References 31 publications

Fucoxanthin Prevents 6‐OHDA‐Induced Neurotoxicity by Targeting Keap1

Fucoxanthin Prevents 6‐OHDA‐Induced Neurotoxicity by Targeting Keap1

Heme Oxygenase-1 Protects Hair Cells From Gentamicin-Induced Death

Ferroptosis and its role in skeletal muscle diseases

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