Anti-inflammatory effects of Aureusidin in LPS-stimulated RAW264.7 macrophages via suppressing NF-κB and activating ROS- and MAPKs-dependent Nrf2/HO-1 signaling pathways

Ren, Jie; Su, Dan; Li, Lixia; Cai, H.; Zhang, Meiju; Zhai, Jingchen; Li, Minyue; Wu, Xinyue; Hu, Kun

doi:10.1016/j.taap.2019.114846

Cited by 141 publications

(88 citation statements)

References 35 publications

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“…However, recent data has shown that, in some cases, ROS might also participate in anti-inflammatory responses. Aureusidin, a natural flavonoid, presented anti-inflammatory effects in LPS-stimulated RAW 264.7 macrophages by increasing cellular ROS levels [27]. Previous studies have demonstrated the relevant involvement of other NOX isoforms, mainly NOX2, in COX-2 activation [14][15][16].…”

Section: Discussionmentioning

confidence: 99%

Induction of Cyclooxygenase-2 by Overexpression of the Human NADPH Oxidase 5 (NOX5) Gene in Aortic Endothelial Cells

Marqués

Cortés

Pejenaute

et al. 2020

Cells

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Oxidative stress is a main molecular mechanism that underlies cardiovascular diseases. A close relationship between reactive oxygen species (ROS) derived from NADPH oxidase (NOX) activity and the prostaglandin (PG) biosynthesis pathway has been described. However, little information is available about the interaction between NOX5 homolog-derived ROS and the PG pathway in the cardiovascular context. Our main goal was to characterize NOX5-derived ROS effects in PG homeostasis and their potential relevance in cardiovascular pathologies. For that purpose, two experimental systems were employed: an adenoviral NOX5-β overexpression model in immortalized human aortic endothelial cells (TeloHAEC) and a chronic infarction in vivo model developed from a conditional endothelial NOX5 knock-in mouse. NOX5 increased cyclooxygenase-2 isoform (COX-2) expression and prostaglandin E2 (PGE2) production through nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in TeloHAEC. Protein kinase C (PKC) activation and intracellular calcium level (Ca++) mobilization increased ROS production and NOX5 overexpression, which promoted a COX-2/PGE2 response in vitro. In the chronic infarction model, mice encoding endothelial NOX5 enhanced the cardiac mRNA expression of COX-2 and PGES, suggesting a COX-2/PGE2 response to NOX5 presence in an ischemic situation. Our data support that NOX5-derived ROS may modulate the COX-2/PGE2 axis in endothelial cells, which might play a relevant role in the pathophysiology of heart infarction.

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Section: Discussionmentioning

confidence: 99%

Induction of Cyclooxygenase-2 by Overexpression of the Human NADPH Oxidase 5 (NOX5) Gene in Aortic Endothelial Cells

Marqués

Cortés

Pejenaute

et al. 2020

Cells

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“…The MAP kinase-interacting kinases (MNK1 and MNK2) are serine threonine kinases which are activated by MAPKs, regulating protein synthesis by phosphroylating eukaryotic translation initiation factor 4E (eIF4E) [27] , [28] , [29] . Although numerous studies have shown that MAPK pathways are involved in the anti-inflammatory and tissue injury preventing processes [30] , the role of MNKs in ALI has remained relatively unexplored until now. Here, we investigated whether partial inhibition of MAPK pathways by targeting MNKs was effective in the prevention and treatment of ALI, and potential mechanisms that might be involved.…”

Section: Introductionmentioning

confidence: 99%

MNK as a potential pharmacological target for suppressing LPS-induced acute lung injury in mice

Gao

Teng

Yang

et al. 2021

Biochemical Pharmacology

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“…The MAPK family is involved in transmitting signals from various extracellular ligands and converting them into a wide range of intracellular responses [ 29 ]. The MAPK family plays a crucial role in proinflammatory responses [ 30 ]. After human buccal mucosal fibroblasts were treated with PD98059, the inhibitor of ERK activation reduced the NF-κB expression induced by safrole.…”

Section: Discussionmentioning

confidence: 99%

Safrole-induced expression of proinflammatory responses is associated with phosphorylation of mitogen-activated protein kinase family and the nuclear factor-κB/inhibitor of κB pathway in macrophages

Shen

Lee

et al. 2020

Tzu Chi Med J

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Objective: Safrole, also called shikimol and Sassafras, is the carcinogenic and phenylpropanoid compound extracted from Sassafras tree and anise, betel, and camphor. Moreover, a high concentration of safrole can be occur in the saliva because of betel nut or areca quid chewing which a common habit observed in Southern and Southeastern Asia. Notably, macrophages are crucial phagocytic cells of the immune system. Nonetheless, to date, no evidence has been reported regarding safrole-induced proinflammatory response and the corresponding mechanism in macrophages. Materials and Methods: In the present study, the cytokines expression, NO generation, protein phosphorylation, and expression were assessed by enzyme-linked immunosorbent assay, Griess reagent, and Western blot assay, respectively. Results: In this study, we determined that safrole induces the generation of nitric oxide and proinflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, and IL-6 in RAW264.7 macrophages in a concentration-dependent manner. Furthermore, inhibitor of κB (IκB) degradation was caused by safrole in a concentration-dependent manner. In addition, the phosphorylation of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) family, including p38 MAPK, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase, was induced by safrole began to increase at 10 μM and attained a plateau at 100 μM. Conclusion: These results indicated that safrole induces the expression of proinflammatory responses in macrophages through the NF-κB/IκB pathway and its upstream factor, MAPK family phosphorylation.

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Anti-inflammatory effects of Aureusidin in LPS-stimulated RAW264.7 macrophages via suppressing NF-κB and activating ROS- and MAPKs-dependent Nrf2/HO-1 signaling pathways

Cited by 141 publications

References 35 publications

Induction of Cyclooxygenase-2 by Overexpression of the Human NADPH Oxidase 5 (NOX5) Gene in Aortic Endothelial Cells

Induction of Cyclooxygenase-2 by Overexpression of the Human NADPH Oxidase 5 (NOX5) Gene in Aortic Endothelial Cells

MNK as a potential pharmacological target for suppressing LPS-induced acute lung injury in mice

Safrole-induced expression of proinflammatory responses is associated with phosphorylation of mitogen-activated protein kinase family and the nuclear factor-κB/inhibitor of κB pathway in macrophages

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