Quercetin-3-O-β-D-Glucuronide Suppresses Lipopolysaccharide-Induced JNK and ERK Phosphorylation in LPS-Challenged RAW264.7 Cells

Park, Jin‐Young; Lim, Man Sup; Kim, Song-In; Lee, Hee Jae; Kim, Sung‐Soo; Kwon, Yong-Soo; Wang, Chun

doi:10.4062/biomolther.2016.026

Cited by 31 publications

(19 citation statements)

References 31 publications

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“…Quercetin suppresses the LPS-induced inflammatory response via various mechanisms [18,22,27,28]; e.g., by inhibiting the NF-κB, STAT-1, and Syk/Src/IRAK-1 pathways. However, little is known about the effect of quercetin on cell motility.…”

Section: Discussionmentioning

confidence: 99%

Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton

Cui

Wang

et al. 2018

Cell Adhesion & Migration

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The natural flavonoid quercetin has antioxidant, anti-inflammatory, and anticancer effects. We investigated the effect of quercetin on lipopolysaccharide (LPS)-induced macrophage migration. Quercetin significantly attenuated LPS-induced inducible nitric oxide synthase (iNOS)-derived nitric oxide (NO) production in RAW264.7 cells without affecting their viability. Additionally, quercetin altered the cell size and induced an elongated morphology and enlarged the vacuoles and concentrated nuclei. Quercetin significantly disrupted the F-actin cytoskeleton structure. Furthermore, quercetin strongly inhibited LPS-induced macrophage adhesion and migration in a dose-dependent manner. Moreover, quercetin inhibited the LPS-induced expression of p-FAK, p-paxillin, FAK, and paxillin as well as the cytoskeletal adapter proteins vinculin and Tensin-2. Therefore, quercetin suppresses LPS-induced migration by inhibiting NO production, disrupting the F-actin cytoskeleton, and suppressing the FAK-paxillin pathway. Quercetin may thus have potential as a therapeutic agent for chronic inflammatory diseases.

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Section: Discussionmentioning

confidence: 99%

Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton

Cui

Wang

et al. 2018

Cell Adhesion & Migration

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“…These results indicate that RAC selectively regulates signaling molecules, ERK and NF-κB. There are some studies showing that selective inhibition of ERK and NF-κB could not affect the production of TNF-α but decreased other inflammatory mediators, such as IL-1β, IL-6, iNOS and COX2 [ 41 , 42 , 43 ]. It has also been reported that selective inhibition of p38 or JNK downregulated TNF-α as well as other inflammatory mediators [ 44 ].…”

Section: Resultsmentioning

confidence: 84%

Retrofractamide C Derived from Piper longum Alleviates Xylene-Induced Mouse Ear Edema and Inhibits Phosphorylation of ERK and NF-κB in LPS-Induced J774A.1

et al. 2020

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Many studies have reported the biological activities of retrofractamide C (RAC). However, few studies have investigated the anti-inflammatory effect of RAC. In the present study, we investigated the anti-inflammatory effect of RAC using lipopolysaccharide (LPS)-induced J774A.1 cells and a xylene-induced mouse ear edema model. Treatment with RAC decreased LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) secretion and inducible NO synthase (iNOS) and cyclooxygenase 2 (COX2) protein expression. It also downregulated the LPS-induced production of interleukin-1β (IL-1β) and interleukin-6 (IL-6) but not tumor necrosis factor α (TNF-α). In the LPS-induced signaling pathway, RAC inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB) but not c-Jun N-terminal kinase (JNK) or p38. In a xylene-induced mouse ear edema model, RAC treatment alleviated edema formation and inflammatory cell infiltration. In conclusion, the present study indicates that RAC has the potential to have anti-inflammatory effects and could be a prospective functional food.

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“…BMMs were seeded into 96-well plates (8 × 10 3 cells/well) in triplicate, and cultured in complete α-MEM (10% FBS and 30 ng/ml M-CSF) with isorhamnetin 3-O-neohesperidoside at a concentration (0.5, 1, 5, 10, 25, 50, 100 and 200 μM) for 24, 72, and 96 hrs. Ten microliters of CCK-8 solution was added to each well for 4 h, following which cell viability was determined by measuring the absorbance at 450 nm, as reported previously 16 . www.nature.com/scientificreports www.nature.com/scientificreports/ Osteoclast differentiation and TRAP staining.…”

Section: Discussionmentioning

confidence: 99%

“…www.nature.com/scientificreports www.nature.com/scientificreports/ Osteoclast differentiation and TRAP staining. As reported previously 16 , BMMs were seeded into 96-well plates (1 × 10 4 cells/well). After 24 h, the cells were cultured in α-MEM (10% FBS, 30 ng/ml M-CSF and 50 ng/mL RANKL) with isorhamnetin 3-O-neohesperidoside at a concentration gradient (0, 1, 5, 25 and 50 μM).…”

Section: Discussionmentioning

confidence: 99%

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Isorhamnetin 3-O-neohesperidoside promotes the resorption of crown-covered bone during tooth eruption by osteoclastogenesis

Zheng

Shang

et al. 2020

Sci Rep

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Delayed resorption of crown-covered bone is a critical cause of delayed tooth eruption. Traditional herbal medicines may be good auxiliary treatments to promote the resorption of crown-covered bone. This study was carried out to analyse the effect of isorhamnetin 3-O-neohesperidoside on receptor activator of nuclear factor-kB ligand (RANKL)-induced osteoclastogenesis in vitro and resorption of the crown-covered bone of the lower first molars in mice in vivo. Isorhamnetin 3-O-neohesperidoside promoted osteoclastogenesis and the bone resorption of mouse bone marrow macrophages (BMMs) and upregulated mRNA expression of the osteoclast-specific genes cathepsin K (CTSK), vacuolartype H +-ATPase d2(V-ATPase d2), tartrate resistant acid phosphatase (TRAP) and nuclear factor of activated T-cells cytoplasmic 1 (NFATc1). NFATc1, p38 and AKT signalling was obviously activated by isorhamnetin 3-O-neohesperidoside in osteoclastogenesis. Isorhamnetin 3-O-neohesperidoside aggravated resorption of crown-covered bone in vivo. In brief, isorhamnetin 3-O-neohesperidoside might be a candidate adjuvant therapy for delayed intraosseous eruption. The development of osseous eruption is an indispensable stage in the tooth eruption process 1,2. Osteoclast differentiation is stimulated, causing the resorption of crown-covered bone of an erupting tooth, which forms an intraosseous eruption canal 3. Osteoclastogenesis in the crown-covered bone is essential. Impaired osseous eruption, in which osteoclastogenesis is disturbed, is common in clinical practice 4 and can manifest as either delayed or the complete absence of eruption 5,6. Although unerupted teeth are usually asymptomatic, they may cause cosmetic and pathologic complications 4 Treatments include orthodontic uprighting, surgical-orthodontic uprighting, surgical uprighting, surgical repositioning, surgical exposure or the removal of pathologic conditions 7. However, these treatments are very complex and invasive. Research shows that osteoclastogenesis is regulated by a key factor termed receptor activator of NF-κB ligand (RANKL). RANKL agonists or osteoclastogenesis-related drugs can be used to treat delayed tooth eruption 8,9. Traditional Chinese medicine, which is without toxic side effects may also be a good auxiliary treatment for delayed tooth eruption. Isorhamnetin 3-O-neohesperidin, known as Pu huang in Chinese 10 , is the main active substance of T. angustifolia, can also be isolated from the leaves of Acacia salicina 11. Because of its antioxidant, antiatherogenic and anti-inflammatory activities, Pu Huang has been widely used for the treatment of haematuria, dysmenorrhea, uterine bleeding and trauma in China for a long time 12. Isorhamnetin 3-O-neohesperidin has been reported to protect cells against oxidative stress by inhibiting H 2 O 2-induced genotoxicity and DNA damage induced by hydroxyl radicals 13. Intestinal flora including Escherichia sp. 23 and sp. 30, can convert isorhamnetin 3-O-neohesperidin to three main metabolites, isorhamnetin-3-O-glucoside(I3OG), isorhamnet...

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Quercetin-3-O-β-D-Glucuronide Suppresses Lipopolysaccharide-Induced JNK and ERK Phosphorylation in LPS-Challenged RAW264.7 Cells

Cited by 31 publications

References 31 publications

Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton

Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton

Retrofractamide C Derived from Piper longum Alleviates Xylene-Induced Mouse Ear Edema and Inhibits Phosphorylation of ERK and NF-κB in LPS-Induced J774A.1

Isorhamnetin 3-O-neohesperidoside promotes the resorption of crown-covered bone during tooth eruption by osteoclastogenesis

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