β‐Asarone suppresses TNF‐α expression through DNA methylation and c‐Jun‐mediated transcription modulation in scratch‐injured neuronal cells

Yi, Min; Wang, Dongsheng; Chen, Yanyi; Xu, Xia; Dai, Xing-Ping

doi:10.1002/jbt.22798

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…These results demonstrate that rTNF-α may be a critical regulator of the barrier that prevents cytotoxic molecules from entering the fetal circulation. Accumulating evidence demonstrates that in cancers, TNF-α stimulates c-Jun through the activation of c-Jun N-terminal kinase (JNK), which is a classical signaling pathway tightly associated with inflammation (18). In this study, we analyzed c-Jun mRNA and protein levels in response to rTNF-α treatment and found that rTNF-α induced c-Jun expression and phosphorylation in a doseand time-dependent manner in Bewo cells, consistent with previous reports demonstrating that TNF-α facilitates a variety of pathophysiological activities through transcriptional and posttranscriptional regulation of c-Jun expression (19,20).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory factor tumor necrosis factor-α (TNF-α) activates P-glycoprotein (P-gp) by phosphorylating c-Jun and thus promotes transportation in placental cells

Li¹,

Yan²,

Li³

et al. 2022

Transl Pediatr

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Background: P-glycoprotein (P-gp), encoded by the ABCB1 gene, actively pumps drugs and other xenobiotics from trophoblast cells back into the maternal circulation and thus acts as one of the most critical protectors of the fetus. The effect of tumor necrosis factor-α (TNF-α) on P-gp and molecule-transporting activity remains unknown. The goal of this study was to investigate the role of TNF-α in placental moleculetransporting activity and the underlies mechanisms.Methods: Cultured human placental choriocarcinoma cell lines, Bewo, JEG-3 and JAR, were used in this study.Cultured cells were incubated with 5, 10 and 20 ng/mL of recombinant TNF-α (rTNF-α) for 24 h, respectively, for follow-up experiments. The dimer form and expression of activator protein-1 (AP-1) family members were detected using Western blot (WB) and chromatin immunoprecipitation (ChIP). mRNA and protein expression of ABCB1 were detected using reverse transcriptional quantitative polymerase chain reaction (RT-qPCR) and WB, respectively. Double luciferase labeling was used to verify the concentration of digoxin. Electromobility shift assay (EMSA) and ChIP were used to identify the binding ability of c-Jun to ABCB1 gene promoter. Proliferation and apoptosis of Bewo cells were determined using flow cytometry. Digoxin concentration were determined using dual luciferase labeling method.Results: Administration of rTNF-α upregulated the expression of c-Jun but not JunB or JunD in a dosedependent manner and promoted the binding of c-Jun to the ABCB1 promoter region in Bewo cells. rTNF-α also increased the uptake of two P-gp-specific substrates, Rh123 and DiOC 2 (3), a function reversed by the addition of SP600125 and SR11302. We also found that rTNF-α increased the efflux ratio of digoxin, an outcome that was reversed, as expected, by inhibiting c-Jun and P-gp binding activities. Furthermore, we identified that rTNF-α tightly regulates the molecule-transporting activity of P-gp by promoting the phosphorylation of c-Jun.Conclusions: TNF-α activates P-gp to promote placental molecule-transporting activity by directly upregulating c-Jun expression and phosphorylation. These findings demonstrate the clinical significance of TNF-α in modulating the placental barrier, which plays an important role in protecting fetus against harmful drugs.

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Section: Discussionmentioning

confidence: 99%

Inflammatory factor tumor necrosis factor-α (TNF-α) activates P-glycoprotein (P-gp) by phosphorylating c-Jun and thus promotes transportation in placental cells

Li¹,

Yan²,

Li³

et al. 2022

Transl Pediatr

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“…Beta-asarone represents the cis isomer of asarone. Recent findings suggest that this phenylpropanoid can regulate different molecular mechanisms to retrieve axonal regeneration and apoptosis in mouse primary cortical neurons after scratch injury damage [129]. In detail, β-asarone can inhibit JNK-dependent c-jun phosphorylation and activation, which ultimately is unable to interact with the promoter region of the TNF-α gene to stimulate its transcription.…”

Section: Acorus Tatarinowii Eomentioning

confidence: 99%

“…In detail, β-asarone can inhibit JNK-dependent c-jun phosphorylation and activation, which ultimately is unable to interact with the promoter region of the TNF-α gene to stimulate its transcription. Moreover, β-asarone induces the upregulation of UHFR1 protein that, in turn, recruits DNA methyltransferase 1 to induce TNF-α promoter methylation and thus gene expression silencing [129].…”

Section: Acorus Tatarinowii Eomentioning

confidence: 99%

Management of the Brain: Essential Oils as Promising Neuroinflammation Modulator in Neurodegenerative Diseases

Avola,

Furnari,

Graziano

et al. 2024

Antioxidants

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Neuroinflammation, a pivotal factor in the pathogenesis of various brain disorders, including neurodegenerative diseases, has become a focal point for therapeutic exploration. This review highlights neuroinflammatory mechanisms that hallmark neurodegenerative diseases and the potential benefits of essential oils in counteracting neuroinflammation and oxidative stress, thereby offering a novel strategy for managing and mitigating the impact of various brain disorders. Essential oils, derived from aromatic plants, have emerged as versatile compounds with a myriad of health benefits. Essential oils exhibit robust antioxidant activity, serving as scavengers of free radicals and contributing to cellular defense against oxidative stress. Furthermore, essential oils showcase anti-inflammatory properties, modulating immune responses and mitigating inflammatory processes implicated in various chronic diseases. The intricate mechanisms by which essential oils and phytomolecules exert their anti-inflammatory and antioxidant effects were explored, shedding light on their multifaceted properties. Notably, we discussed their ability to modulate diverse pathways crucial in maintaining oxidative homeostasis and suppressing inflammatory responses, and their capacity to rescue cognitive deficits observed in preclinical models of neurotoxicity and neurodegenerative diseases.

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“…Previous studies have shown that β-asarone exhibits good pharmacological effects on the astrocyte-neuronal cell system. Our research team previously found that β-asarone ether exerts a protective effect on PC12 cell injury induced by amyloid β 1-42 (Aβ 1-42 )-activated astrocytes [8], which was con rmed by Zhenwan Li and Yi M [9,10]. However, the mechanism underlying the β-asarone-mediated regulation of astrocyte-neuron system is not clear yet.…”

Section: Introductionmentioning

confidence: 99%

β-asarone inhibits autophagic neuron death by downregulating reactive astrocytes-derived SPARC expression in LPS-induced SH-SY5Y cells

Huang

Wang

Huang

et al. 2023

Preprint

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β-asarone, the main active component of Acori tatarinowii rhizoma (ATR), exhibits several pharmacological properties, including anti-inflammatory, anti-aging, and neuroprotective effects. In recent years, a large number of studies have shown that β-asarone exerts a positive effect on improving the cognitive level of individuals with Alzheimer’s disease (AD). However, the effects of β-asarone on autophagy in neuroinflammation-induced AD and the potential underlying mechanisms remain unclear. In the present study, we found that β-asarone inhibited LPS-induced activation of NHA cells and significantly decreased the expression of inflammatory factors and sparc. Exposure to exogenous SPARC promoted apoptosis and autophagy in neuronal cells. Further, we co-cultured LPS-induced reactive human astrocytes [NHA (normal human astrocytes)] with human neuronal cells (SH-SY5Y cell line) to establish a neurocyte inflammatory microenvironment to mimic the neuroinflammatory model of AD in vitro. Based on the above co-culture system, we observed that after SPARC overexpression in NHA, the behavior of the neuronal cells resembled that after exogenous SPARC treatment. However, β-asarone treatment reversed these effects and protected the cells against neuronal damage. These findings suggested that the matrix protein SPARC plays an important role in neuronal damage in AD model mice, and β-asarone intervention can be utilized as a potential therapeutic strategy for AD.

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β‐Asarone suppresses TNF‐α expression through DNA methylation and c‐Jun‐mediated transcription modulation in scratch‐injured neuronal cells

Cited by 5 publications

References 23 publications

Inflammatory factor tumor necrosis factor-α (TNF-α) activates P-glycoprotein (P-gp) by phosphorylating c-Jun and thus promotes transportation in placental cells

Inflammatory factor tumor necrosis factor-α (TNF-α) activates P-glycoprotein (P-gp) by phosphorylating c-Jun and thus promotes transportation in placental cells

Management of the Brain: Essential Oils as Promising Neuroinflammation Modulator in Neurodegenerative Diseases

β-asarone inhibits autophagic neuron death by downregulating reactive astrocytes-derived SPARC expression in LPS-induced SH-SY5Y cells

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