Anti-inflammatory effects of vanadium-binding protein from Halocynthia roretzi in LPS-stimulated RAW264.7 macrophages through NF-κB and MAPK pathways

Kim, Aaron Taehwan; Kim, Dae‐Ok

doi:10.1016/j.ijbiomac.2019.04.106

Cited by 21 publications

(15 citation statements)

References 40 publications

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“…Activation of c-Jun N-terminal kinase (JNK) has been reported in APPSwe/PS1dE9 mice to induce long-term synaptic toxicity and cognition impairment (Fang et al, 2017;Liang et al, 2019). Vanadium was demonstrated to decrease phosphorylation of JNK (p-JNK) and thus reduce JNK activation (Wang et al, 2015;Kim and Kim, 2019). To further evaluate the role of BEOV on decreased synapses, JNK expression and phosphorylated JNK levels were analyzed in both hippocampus and cortex of APPSwe/PS1dE9 mice.…”

Section: Beov Protected Hippocampal and Cortical Synapses Of Ad Modelmentioning

confidence: 99%

The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer’s Disease in APPSwe/PS1dE9 Mice

Han

Zhu

et al. 2020

Front. Mol. Neurosci.

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Alzheimer's disease (AD) is a widely distributed neurodegenerative disease characterized clinically by cognitive deficits and pathologically by formation of amyloid-β (Aβ) plaque and neurofibrillary tangles (NFTs) in the brain. Vanadium is a biological trace element that has a function to mimic insulin for diabetes. Bis(ethylmaltolato) oxidovanadium (IV) (BEOV) has been reported to have a hypoglycemic property, but its effect on AD remains unclear. In this study, BEOV was supplemented at doses of 0.2 and 1.0 mmol/L to the AD model mice APPSwe/PS1dE9 for 3 months. The results showed that BEOV substantially ameliorated glucose metabolic disorder as well as synaptic and behavioral deficits of the AD mice. Further investigation revealed that BEOV significantly reduced Aβ generation by increasing the expression of peroxisome proliferator-activated receptor gamma and insulin-degrading enzyme and by decreasing β-secretase 1 in the hippocampus and cortex of AD mice. BEOV also reduced tau hyperphosphorylation by inhibiting protein tyrosine phosphatase-1B and regulating the pathway of insulin receptor/insulin receptor substrate-1/protein kinase B/glycogen synthase kinase 3 beta. Furthermore, BEOV could enhance autophagolysosomal fusion and restore autophagic flux to increase the clearance of Aβ deposits and phosphorylated tau in the brains of AD mice. Collectively, the present study provides solid data for revealing the function and mechanism of BEOV on AD pathology.

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Section: Beov Protected Hippocampal and Cortical Synapses Of Ad Modelmentioning

confidence: 99%

The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer’s Disease in APPSwe/PS1dE9 Mice

Han

Zhu

et al. 2020

Front. Mol. Neurosci.

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“…NF-kB and MAPK are also important signaling pathways that affect foam cell aggregation and inflammatory response (Kim and Kim, 2019;Shen W. et al, 2019). Previous studies have demonstrated that NF-kB is a key regulator of macrophage inflammation, and NF-kB inhibition reduces foam cell formation (Plotkin et al, 2017;Islam et al, 2018;Adam et al, 2019;Kim and Kim, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…NF-κB and MAPK are also important signaling pathways that affect foam cell aggregation and inflammatory response ( Kim and Kim, 2019 ; Shen W. et al, 2019 ). Previous studies have demonstrated that NF-κB is a key regulator of macrophage inflammation, and NF-κB inhibition reduces foam cell formation ( Plotkin et al, 2017 ; Islam et al, 2018 ; Adam et al, 2019 ; Kim and Kim, 2019 ). The current study showed that CK significantly inhibited phosphorylation of IKKβ and suppressed IκBα degradation and phosphorylation, thereby reducing the phosphorylation of NF-κB P65.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Compound K Attenuates Ox-LDL-Mediated Macrophage Inflammation and Foam Cell Formation via Autophagy Induction and Modulating NF-κB, p38, and JNK MAPK Signaling

Luo

Sun

2020

Front. Pharmacol.

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Atherosclerosis is a major reason for the high morbidity and mortality of cardiovascular diseases. Macrophage inflammation and foam cell formation are the key pathological processes of atherosclerosis. Ginsenoside compound K (CK) is a metabolite derived from ginseng. CK has anti atherosclerotic effect, but the molecular mechanism remains to be elucidated. We aim to explore the protective effect of CK against ox-LDL-induced inflammatory responses and foam cells formation in vitro and explore its potential mechanisms. Through the results of oil red O staining, Western blot, and qPCR, we found that CK significantly inhibited the foam cell formation, reduced the expression of SR-A1 and increased ABCA1 and ABCG1 expression. In addition, CK increased the number of autophagosomes and upregulated the LC3II/LC3I ratio and the expressions of ATG5 and Beclin-1 but decreased p62 expression. Moreover, CK significantly inhibited the NF-kB, p38, and JNK MAPK signaling pathway. Altogether, CK attenuated macrophage inflammation and foam cell formation via autophagy induction and by modulating NF-kB, p38, and JNK MAPK signaling. Thus, CK has potential as a therapeutic drug for atherosclerosis.

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“…ABTS, 1,1‐diphenyl‐2‐picrylhydrazyl (DPPH), p ‐nitrophenyl‐α‐D‐glucopyranoside ( p NPG), α‐glucosidase from Bacillus stearothermophilus, and Saccharomyces cerevisiae , intestinal acetone powders from rat, α‐amylase from porcine pancreas, G‐6‐Pase and glucose (GO) assay kit were purchased from Sigma‐Aldrich Chemical Co. (St. Louis, MO, USA). The VBP and trifuhalol A were prepared according to our previous methods (Kim & Kim, 2019; Phasanasophon & Kim, 2018). All other reagents utilized in the present study were of analytical grade.…”

Section: Methodsmentioning

confidence: 99%

“…Vanadium distributes widely in nature and exhibits numbers of biological effects (Domingo & Gómez, 2016). A variety of vanadium compounds were confirmed to have antidiabetic, anti‐inflammatory, antiviral, and antibacterial effects (Kim & Kim, 2019; Kumar et al, 2018; Pessoa et al, 2015). It has been reported that inorganic vanadium compound vanadyl sulfate can inhibit G‐6‐Pase (Shehzad, 2013), and sodium metavanadate can reduce basal lipolysis in 3T3‐L1 preadipocytes (Liu et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Antioxidant and antidiabetic activities of vanadium‐binding protein and trifuhalol A

Zhang

Kim

Liu³

et al. 2020

J. Food Biochem.

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Diabetes mellitus has become a major global health problem due to increasing morbidity among all age groups. It has been reported that the number of patients with diabetes was more than 450 million in 2017, and would reach to 693 million on 2045 (Makinde et al., 2019). Diabetes mellitus is considered as a chronic and systemic metabolic disease which is associated with insulin deficiency (type 1) and insulin resistance or insulin insensitiveness (type 2) (Chausmer, 1998; De Liefde et al., 2005). The high blood glucose level could lead to hypertension, hyperlipidemia, weight gain, or obesity (Ahmed et al., 2019). It is well known that the destruction of pancreatic β cells can cause insulin deficiency and further develop into diabetes (Yoon & Jun, 2005). The pancreatic β cells are highly sensitive toward oxidative stress, which

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Anti-inflammatory effects of vanadium-binding protein from Halocynthia roretzi in LPS-stimulated RAW264.7 macrophages through NF-κB and MAPK pathways

Cited by 21 publications

References 40 publications

The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer’s Disease in APPSwe/PS1dE9 Mice

The Protective Effect of Vanadium on Cognitive Impairment and the Neuropathology of Alzheimer’s Disease in APPSwe/PS1dE9 Mice

Ginsenoside Compound K Attenuates Ox-LDL-Mediated Macrophage Inflammation and Foam Cell Formation via Autophagy Induction and Modulating NF-κB, p38, and JNK MAPK Signaling

Antioxidant and antidiabetic activities of vanadium‐binding protein and trifuhalol A

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