Anti-neuroinflammatory effects of citreohybridonol involving TLR4-MyD88-mediated inhibition of NF-кB and MAPK signaling pathways in lipopolysaccharide-stimulated BV2 cells

Cho, Kwang Ho; Kim, Dongcheol; Yoon, Chi–Su; Ko, Won Min; Lee, Seung Jun; Sohn, Jae Hak; Jang, Jae‐Hyuk; Ahn, Jong Seog; Kim, Youn‐Chul; Oh, Hyuncheol

doi:10.1016/j.neuint.2015.12.010

Cited by 46 publications

(35 citation statements)

References 42 publications

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“…A variety of phytochemicals have exhibited anti‐inflammatory effects by inhibiting the production and release of proinflammatory cytokines and mediators (Cho et al, ). Quercetin and catechin are common bioflavonoids found abundantly in fruits and vegetables such as apples, tea, onion, and berries, which are linked to diverse medicinal effects, including anti‐inflammatory, antitumor, antioxidant, and anticarcinogenic activities (Formica & Regelson, ; Wang, Sun‐Waterhouse, Li, Xin, & Li, ).…”

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confidence: 99%

Synergistic anti‐inflammatory effects of quercetin and catechin via inhibiting activation of TLR4–MyD88‐mediated NF‐κB and MAPK signaling pathways

Liu³

et al. 2019

Phytotherapy Research

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The synergistic anti‐inflammatory effect of quercetin and catechin was investigated using lipopolysaccharide (LPS)‐stimulated macrophage RAW 264.7 cells. Results showed that the combined treatment of quercetin with catechin synergistically attenuated LPS‐stimulated increase of some proinflammatory molecules, including nitric oxide, tumor necrosis factor α, interleukin‐1β, nitric oxide synthase, and cyclooxygenase‐2. Moreover, it exhibited significantly (p < 0.05) stronger inhibitory effect on nuclear translocation of nuclear factor‐κB (NF‐κB) by suppressing the phosphorylation of NF‐κB p65 and p50 submits and on the phosphorylation of ETS domain‐containing protein and c‐Jun N‐terminal kinase than any of quercetin or catechin alone. Besides, the cotreatment of quercetin with catechin significantly (p < 0.05) restored the impaired expression of toll‐like receptor 4, myeloid differentiation primary response gene 88, and some downstream effectors (IRAK1, TRAF6, and TAK1). These results suggest that quercetin and catechin possessed synergistic anti‐inflammatory effects, which may be attributed to their roles in suppressing the activation of TLR4–MyD88‐mediated NF‐κB and mitogen‐activated protein kinases signaling pathways.

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confidence: 99%

Synergistic anti‐inflammatory effects of quercetin and catechin via inhibiting activation of TLR4–MyD88‐mediated NF‐κB and MAPK signaling pathways

Liu³

et al. 2019

Phytotherapy Research

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“…MAPK/ErK signaling is an integral part of TLR4 activation associated with neuroinflammatory responses in the CNS (Badshah et al, 2016 ; Cho et al, 2016 ). Furthermore, MAPK/ErK activation, downstream of TLR4, may contribute to the phosphorylation (inactivation) of CaMKIIα at post-synaptic sites (Liu et al, 2010 ; Li et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

“…The relative abundance of β ARs on various cell types in the nervous and vascular system makes it (that is β ARs ) a suitable target for disease models and therapeutic targeting (Badshah et al, 2016 ; Ranjan et al, 2016 ). Furthermore, activation of Ras/Raf -downstream of β ARs -suggests the involvement of pro-inflammatory receptors and associated pathways in systemic cardiovascular changes (Cho et al, 2016 ). Although previous studies have described changes in systemic inflammatory response in heart failure models, how a systemic driven change may affect the neurochemical architecture of the preautonomic centers is yet to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

Systemic Sympathoexcitation Was Associated with Paraventricular Hypothalamic Phosphorylation of Synaptic CaMKIIα and MAPK/ErK

et al. 2017

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Systemic administration of adrenergic agonist (Isoproterenol; ISOP) is known to facilitate cardiovascular changes associated with heart failure through an upregulation of cardiac toll-like receptor 4 (TLR4). Furthermore, previous studies have shown that cardiac tissue-specific deletion of TLR4 protects the heart against such damage. Since the autonomic regulation of systemic cardiovascular function originates from pre-autonomic sympathetic centers in the brain, it is unclear how a systemically driven sympathetic change may affect the pre-autonomic paraventricular hypothalamic nuclei (PVN) TLR4 expression. Here, we examined how change in PVN TLR4 was associated with alterations in the neurochemical cytoarchitecture of the PVN in systemic adrenergic activation. After 48 h of intraperitoneal 150 mg/kg ISOP treatment, there was a change in PVN CaMKIIα and MAPK/ErK expression, and an increase in TLR4 in expression. This was seen as an increase in p-MAPK/ErK, and a decrease in synaptic CaMKIIα expression in the PVN (p < 0.01) of ISOP treated mice. Furthermore, there was an upregulation of vesicular glutamate transporter (VGLUT 2; p < 0.01) and a decreased expression of GABA in the PVN of Isoproterenol (ISOP) treated WT mice (p < 0.01). However, after a PVN-specific knockdown of TLR4, the effect of systemic administration of ISOP was attenuated, as indicated by a decrease in p-MAPK/ErK (p < 0.01) and upregulation of CaMKIIα (p < 0.05). Additionally, loss of inhibitory function was averted while VGLUT2 expression decreased when compared with the ISOP treated wild type mice and the control. Taken together, the outcome of this study showed that systemic adrenergic activation may alter the expression, and phosphorylation of preautonomic MAPK/ErK and CaMKIIα downstream of TLR4. As such, by outlining the roles of these kinases in synaptic function, we have identified the significance of neural TLR4 in the progression, and attenuation of synaptic changes in the pre-autonomic sympathetic centers.

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“…TNF-α is a pro-inflammatory cytokine and its overproduction exacerbates different inflammatory conditions including sepsis and rheumatoid arthritis (Cho et al. 2015 ). In this study, comp showed a significant inhibitory effect on the production of TNF-α in CpG DNA-stimulated BMDCs, suggesting that it may have the potential to ameliorate TNF-α-associated diseases.…”

Section: Discussionmentioning

confidence: 99%

3-Hydroxy-4,7-megastigmadien-9-one, isolated from Ulva pertusa , attenuates TLR9-mediated inflammatory response by down-regulating mitogen-activated protein kinase and NF-κB pathways

Ali

Manzoor

Koo

et al. 2016

Pharmaceutical Biology

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Context: Seaweeds are rich in bioactive compounds in the form of vitamins, phycobilins, polyphenols, carotenoids, phycocyanins and polysaccharides; many of these are known to have advantageous applications in human health. 3-Hydroxy-4,7-megastigmadien-9-one (comp) was isolated from Ulva pertusa (U. pertusa) Kjellman (Ulvaceae), which is a familiar edible green seaweed.Objective: This study evaluates the anti-inflammatory activity of comp in CpG DNA-stimulated bone marrow-derived dendritic cells (BMDCs).Materials and methods: For evaluating the effect of comp on cytokines production, BMDCs were treated with doses of comp (0, 0.5, 1, 2, 5, 10, 25 and 50 μM) for 1 h before stimulation with CpG DNA (1 μM). Cytokine production was measured by ELISA. Western blotting was conducted for evaluating effect of comp (50 μM) on MAPKs and NF-κB pathways. Luciferase reporter gene assay was conducted for effect of comp (0, 5, 10 and 25 μM) on transcriptional activity of AP-1 and NF-κB.Results: Comp exhibited strong inhibition of interleukin (IL)-12 p40, IL-6 and TNF-α cytokine production with IC50 values of 6.02 ± 0.35, 27.14 ± 0.73, and 7.56 ± 0.21 μM, respectively. It blocked MAPKs and NF-κB pathways by inhibiting the phosphorylation of ERK1/2, JNK1/2, p38 and IκBα. In addition, it strongly inhibited the transcriptional activity of AP-1 and NF-κB with IC50 values of 8.74 ± 0.31 and 12.08 ± 0.24 μM, respectively.Discussion and conclusion: Taken together, these data suggest that comp has a significant anti-inflammatory property and warrants further studies concerning the potential of comp for medicinal use.

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Anti-neuroinflammatory effects of citreohybridonol involving TLR4-MyD88-mediated inhibition of NF-кB and MAPK signaling pathways in lipopolysaccharide-stimulated BV2 cells

Cited by 46 publications

References 42 publications

Synergistic anti‐inflammatory effects of quercetin and catechin via inhibiting activation of TLR4–MyD88‐mediated NF‐κB and MAPK signaling pathways

Synergistic anti‐inflammatory effects of quercetin and catechin via inhibiting activation of TLR4–MyD88‐mediated NF‐κB and MAPK signaling pathways

Systemic Sympathoexcitation Was Associated with Paraventricular Hypothalamic Phosphorylation of Synaptic CaMKIIα and MAPK/ErK

3-Hydroxy-4,7-megastigmadien-9-one, isolated from Ulva pertusa , attenuates TLR9-mediated inflammatory response by down-regulating mitogen-activated protein kinase and NF-κB pathways

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