Punicalagin ameliorates collagen-induced arthritis by downregulating M1 macrophage and pyroptosis via NF-κB signaling pathway

Ge, Gaoran; Bai, Jiaxiang; Wang, Qing; Liang, Xiaoyao; Tao, Huaqiang; Chen, Hao; Wei, Minggang; Niu, Junjie; Yang, Huilin; Xu, Yaozeng; Hao, Yuefeng; Xue, Yi; Geng, Dechun

doi:10.1007/s11427-020-1939-1

Cited by 91 publications

(48 citation statements)

References 65 publications

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“…Due to the complex interplay of cytokines, metabolites and limited studies about the macrophages- P gingivalis interaction in tumor microenvironments, future research is expected to decipher it. Although the complexity of M1/M2 ratio, transforming the microglial polarization phenotype in mice models suggested reduced arthritis and learning and memory cognitive deficits ( 56 , 99 , 100 ) proved its therapeutic potentials. Considering the ability of P. gingivalis to induce macrophages M1 polarizations, blocking the macrophages- P gingivalis interaction may be a potential therapeutic method.…”

Section: Discussionmentioning

confidence: 99%

Macrophages: A communication network linking Porphyromonas gingivalis infection and associated systemic diseases

Lin

Huang

et al. 2022

Front. Immunol.

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Porphyromonas gingivalis (P. gingivalis) is a Gram-negative anaerobic pathogen that is involved in the pathogenesis of periodontitis and systemic diseases. P. gingivalis has recently been detected in rheumatoid arthritis (RA), cardiovascular disease, and tumors, as well as Alzheimer’s disease (AD), and the presence of P. gingivalis in these diseases are correlated with poor prognosis. Macrophages are major innate immune cells which modulate immune responses against pathogens, however, multiple bacteria have evolved abilities to evade or even subvert the macrophages’ immune response, in which subsequently promote the diseases’ initiation and progression. P. gingivalis as a keystone pathogen of periodontitis has received increasing attention for the onset and development of systemic diseases. P. gingivalis induces macrophage polarization and inflammasome activation. It also causes immune response evasion which plays important roles in promoting inflammatory diseases, autoimmune diseases, and tumor development. In this review, we summarize recent discoveries on the interaction of P. gingivalis and macrophages in relevant disease development and progression, such as periodontitis, atherosclerosis, RA, AD, and cancers, aiming to provide an in-depth mechanistic understanding of this interaction and potential therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Macrophages: A communication network linking Porphyromonas gingivalis infection and associated systemic diseases

Lin

Huang

et al. 2022

Front. Immunol.

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“…Recently, An et al (2020) and Ge et al (2021) reported that PUN can ameliorate diabetic nephropathy and collagen-induced arthritis by attenuating nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing protein 3 (NLRP3)/caspase-1/gasdermin D (GSDMD)-mediated pyroptosis, respectively. Since that pyroptosis is a form of programmed cell death characterized by gasdermin family protein-mediated pore formation, cellular lysis and the release of IL-1β, Broz et al (2020) and Liu X. et al (2021) propose an idea that PUN is also a pyroptosis inhibitor.…”

Section: Discussionmentioning

confidence: 99%

Punicalagin Alleviates Psoriasis by Inhibiting NF-κB-Mediated IL-1β Transcription and Caspase-1-Regulated IL-1β Secretion

Tang

Zhang

et al. 2022

Front. Pharmacol.

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Psoriasis is a chronic and inflammatory skin disorder characterized by inflammation and epidermal hyperplasia. Punicalagin (PUN) is a main active ingredient of pomegranate (Punica granatum L.) peel with multiple biological activities, such as antibacterial, antioxidant and anti-tumor effects. However, the potential effect of PUN on psoriasis remains unknown. In this study, we want to investigate the pharmacological effect of PUN on psoriasis by using imiquimod (IMQ)-induced psoriatic mice model in vivo and tumor necrosis factor a (TNF-α) and interleukin-17A (IL-17A)-stimulated HaCaT cells in vitro. Our results showed that PUN can effectively alleviate the severity of psoriasis-like symptoms. Mechanistically, PUN potently suppresses the aberrant upregulation of interleukin-1β (IL-1β) and subsequent IL-1β-mediated inflammatory cascade in keratinocytes by inhibiting the nuclear factor kappa B (NF-κB) activation and cleaved caspase-1 expression in vitro and in vivo. Taken together, our findings indicate that PUN can relieve psoriasis by repressing NF-κB-mediated IL-1β transcription and caspase-1-regulated IL-1β secretion, which provide evidence that PUN might represent a novel and promising candidate for the treatment of psoriasis.

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“…Macrophage polarization and cytokine-stimulated ROS in adipose tissue led to glucose intolerance and insulin resistance in obese mice [54]. Macrophages induce pyroptosis by responding to pathogenic microorganisms in the host cytoplasm [55,56]. Moreover, ROS, as secondary messengers, participate in signaling pathway transduction and regulation of M1/M2 macrophage polarization.…”

Section: Discussionmentioning

confidence: 99%

PP1A prevents ROS‐induced pyroptosis by inhibiting MAPK/caspase‐3 in mouse adipose tissue

Chen

Che

et al. 2022

The FEBS Journal

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Pyroptosis is a type of programmed cell death triggered by a variety of exogenous stimuli, playing important roles in the development of cells. Recent studies have shown that pyroptosis also occurs in human and mouse adipocytes. The serine/threonine protein phosphatase 1 catalytic subunit α (PP1A) is located in the nucleus and functions in the regulation of cell development, glucose metabolism and protein synthesis. PP1A can also target important proteins in the process of apoptosis. However, it is still unclear whether PP1A participates in the regulation of pyroptosis in mouse adipocytes. In the present study, we investigated the function of PP1A in reactive oxygen species‐induced pyroptosis and the related mechanism in mouse adipose tissue. Our results demonstrated that PP1A suppressed pyroptosis in adipocytes by inhibiting the reactive oxygen species/mitogen‐activated protein kinase/caspase‐3 signaling pathway and promoting M2 macrophage polarization. This experiment provides a theoretical basis for understanding the regulatory function and mechanism of PP1A in pyroptosis caused by oxidative stress in adipocytes.

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Punicalagin ameliorates collagen-induced arthritis by downregulating M1 macrophage and pyroptosis via NF-κB signaling pathway

Cited by 91 publications

References 65 publications

Macrophages: A communication network linking Porphyromonas gingivalis infection and associated systemic diseases

Macrophages: A communication network linking Porphyromonas gingivalis infection and associated systemic diseases

Punicalagin Alleviates Psoriasis by Inhibiting NF-κB-Mediated IL-1β Transcription and Caspase-1-Regulated IL-1β Secretion

PP1A prevents ROS‐induced pyroptosis by inhibiting MAPK/caspase‐3 in mouse adipose tissue

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