Emodin relieves the inflammation and pyroptosis of lipopolysaccharide-treated 1321N1 cells by regulating methyltransferase-like 3 -mediated NLR family pyrin domain containing 3 expression

Wang, Bu; Liu, Yuan; Jiang, Rui; Liu, Zhiliang; Gao, Haiyun; Chen, Fenqiao; Mei, Jianqiang

doi:10.1080/21655979.2022.2045836

Cited by 19 publications

(22 citation statements)

References 44 publications

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“…Since pyroptosis aggravates CNS injuries-caused secondary injury, m6A modification may attenuate brain damage by suppressing pyroptosis. Consistent with this hypothesis, Wang B. et al (2022) proposed that that in an LPS-induced SBI model, emodin treatment decreased the protein levels of syndecan-1 (SDC-1), NLRP3, caspase-1 and the N-terminal fragment of GSDMD (GSDMD-N) in 1321N1 cells, suggesting that emodin could inhibit pyroptosis. While Nigericin, a NLRP3 activator, reversed the effects of emodin on pyroptosis.…”

Section: Functions Of N6-methyladenosine Modification In Central Nerv...mentioning

confidence: 69%

“…Moreover, emodin up-regulated m6A levels by activation of METTL3, knockdown of METTL3 reversed the effects of emodin on inflammation in SBI. These data demonstrated that emodin inhibited the inflammation of LPS-treated 1321N1 cells by regulation of METTL3 ( Wang B. et al, 2022 ).…”

Section: Functions Of N6-methyladenosine Modification In Central Nerv...mentioning

confidence: 83%

“…Numerous studies have proposed that m6A modification exerted a central effect in CNS injuries-induced inflammation. Wang B. et al (2022) demonstrated that in a sepsis brain injury (SBI) model, lipopolysaccharide (LPS) increased the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and decreased the levels of IL-10 in 1321N1 cells, indicating that LPS treatment induced inflammation in SBI. Treatment of emodin suppressed inflammation as evidenced by decreased levels of TNF-α, IL-1β, IL-6, and increased levels of IL-10 in LPS-treated 1321N1 cells.…”

Section: Functions Of N6-methyladenosine Modification In Central Nerv...mentioning

confidence: 99%

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Crosstalk among N6-methyladenosine modification and RNAs in central nervous system injuries

Tian

Mao

Zhang

2022

Front. Cell. Neurosci.

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Central nervous system (CNS) injuries, including traumatic brain injury (TBI), intracerebral hemorrhage (ICH) and ischemic stroke, are the most common cause of death and disability around the world. As the most common modification on ribonucleic acids (RNAs), N6-methyladenosine (m6A) modification has recently attracted great attentions due to its functions in determining the fate of RNAs through changes in splicing, translation, degradation and stability. A large number of studies have suggested that m6A modification played an important role in brain development and involved in many neurological disorders, particularly in CNS injuries. It has been proposed that m6A modification could improve neurological impairment, inhibit apoptosis, suppress inflammation, reduce pyroptosis and attenuate ferroptosis in CNS injuries via different molecules including phosphatase and tensin homolog (PTEN), NLR family pyrin domain containing 3 (NLRP3), B-cell lymphoma 2 (Bcl-2), glutathione peroxidase 4 (GPX4), and long non-coding RNA (lncRNA). Therefore, m6A modification showed great promise as potential targets in CNS injuries. In this article, we present a review highlighting the role of m6A modification in CNS injuries. Hence, on the basis of these properties and effects, m6A modification may be developed as therapeutic agents for CNS injury patients.

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Section: Functions Of N6-methyladenosine Modification In Central Nerv...mentioning

confidence: 69%

Section: Functions Of N6-methyladenosine Modification In Central Nerv...mentioning

confidence: 83%

Section: Functions Of N6-methyladenosine Modification In Central Nerv...mentioning

confidence: 99%

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Crosstalk among N6-methyladenosine modification and RNAs in central nervous system injuries

Tian

Mao

Zhang

2022

Front. Cell. Neurosci.

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“…Studies have shown that various epigenetic modifications are closely related to the activation or inhibition of pyroptosis and ultimately affect pyroptosis-related diseases, including sepsis. For instance, Wang et al found that emodin could upregulate the expression of methyltransferase-like 3 (METTL3) in sepsisinduced brain injury in vitro, thereby downregulating the mRNA and protein expression of NLRP3 and ultimately inhibiting pyroptosis and inflammation (Wang et al, 2022). In addition, m6A demethylase fat mass and obesity-associated proteins (FTOs) has also been found to regulate pyroptosis in sepsis.…”

Section: Regulation Of Pyroptosis By Epigenetic Modifications In Sepsismentioning

confidence: 99%

Molecular mechanisms and functions of pyroptosis in sepsis and sepsis-associated organ dysfunction

Wen

Liu

Tong

et al. 2022

Front. Cell. Infect. Microbiol.

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Sepsis, a life-threatening organ dysfunction caused by a dysregulated host response to infection, is a leading cause of death in intensive care units. The development of sepsis-associated organ dysfunction (SAOD) poses a threat to the survival of patients with sepsis. Unfortunately, the pathogenesis of sepsis and SAOD is complicated, multifactorial, and has not been completely clarified. Recently, numerous studies have demonstrated that pyroptosis, which is characterized by inflammasome and caspase activation and cell membrane pore formation, is involved in sepsis. Unlike apoptosis, pyroptosis is a pro-inflammatory form of programmed cell death that participates in the regulation of immunity and inflammation. Related studies have shown that in sepsis, moderate pyroptosis promotes the clearance of pathogens, whereas the excessive activation of pyroptosis leads to host immune response disorders and SAOD. Additionally, transcription factors, non-coding RNAs, epigenetic modifications and post-translational modifications can directly or indirectly regulate pyroptosis-related molecules. Pyroptosis also interacts with autophagy, apoptosis, NETosis, and necroptosis. This review summarizes the roles and regulatory mechanisms of pyroptosis in sepsis and SAOD. As our understanding of the functions of pyroptosis improves, the development of new diagnostic biomarkers and targeted therapies associated with pyroptosis to improve clinical outcomes appears promising in the future.

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“…Consequently, in YTHDF1 knockdown mouse brain tissue, the proportion of normal neurons (i.e., those that do not differ from cells exposed to severe sepsis) is significantly increase compared with mice with hyperemia ( 69 ). METTL3 inhibits the inflammation and pyroptosis through decreasing the mRNA stability of NLRP3 in LPS-treated 1321N1 cells, which exhibit a protective effect on SAE ( 70 ).…”

Section: A Methyltransferase Complexmentioning

confidence: 99%

m6A RNA methylation in brain injury and neurodegenerative disease

Deng

Chen

et al. 2022

Front. Neurol.

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N6-methyladenosine (m6A), the most prevalent post-transcriptional RNA modification throughout the eukaryotic transcriptome, participates in diverse biophysiological processes including cell fates, embryonic development and stress responses. Accumulating evidence suggests that m6A modification in neural development and differentiation are highly regulated processes. As RNA m6A is crucial to protein translation and various bioprocesses, its modification dysregulation may also be associated with brain injury. This review highlights the biological significance of m6A modification in neurodegenerative disease and brain injury, including cerebrovascular disorders, is highlighted. Emphasis is placed on recent findings that elucidate the relevant molecular functional mechanism of m6A modification after brain injury and neurodegenerative disease. Finally, a neurobiological basis for further investigation of potential treatments is described.

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Emodin relieves the inflammation and pyroptosis of lipopolysaccharide-treated 1321N1 cells by regulating methyltransferase-like 3 -mediated NLR family pyrin domain containing 3 expression

Cited by 19 publications

References 44 publications

Crosstalk among N6-methyladenosine modification and RNAs in central nervous system injuries

Crosstalk among N6-methyladenosine modification and RNAs in central nervous system injuries

Molecular mechanisms and functions of pyroptosis in sepsis and sepsis-associated organ dysfunction

m6A RNA methylation in brain injury and neurodegenerative disease

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