Grossamide attenuates inflammation by balancing macrophage polarization through metabolic reprogramming of macrophages in mice

Zhao, Wenlong; Xu, Di; Wang, Hong; Zhang, Lin; Wu, Qingqing; Mingzhe, Gao; Wang, Junsong

doi:10.1016/j.intimp.2022.109190

Cited by 7 publications

(5 citation statements)

References 50 publications

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“…We collected cells in the P1 region and used markers for CD206 to distinguish between M0/M1 and M2 and markers for CD80 and CD86 to distinguish between M0 and M1. Of these, M0 cells expressed only CD86 and M1 cells expressed CD80 and CD86 [ 35 ]. In the results, we can see that the untreated HMC3 cells were 8.67% positive for CD206 and showed more polarization in favor of M2.…”

Section: Resultsmentioning

confidence: 99%

Daphnetin Improves Neuropathic Pain by Inhibiting the Expression of Chemokines and Inflammatory Factors in the Spinal Cord and Interfering with Glial Cell Polarization

et al. 2023

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Neuropathic pain (NP) is a common pain disease that seriously affects the quality of life and physical and mental health of patients. Daphnetin is extracted from the Daphne giraldii Nitsche and has the structure of 7,8-dihydroxy coumarin. As a natural product, daphnetin displays a wide range of pharmacological activities, such as analgesia and anti-inflammatory activities, but whether it is able to improve NP through anti-inflammatory effects is unknown. Therefore, this paper intends to investigate the mechanism of daphnetin in improving NP rats affected by the intrathecal injection of tumor necrosis factor-α (TNF-α) from the perspective of anti-inflammation. Our results showed that daphnetin significantly improved hyperalgesia in NP rats. Daphnetin inhibited the activation and polarization of glial cells and neurons in the spinal cord of NP rats and reduced the expression of mRNA and protein of inflammatory factors and chemokine pairs in the spinal cord. Daphnetin inhibited the polarization of human microglia cell 3 (HMC3) cells and human glioma cells (U251) cells toward M1 microglia and A1 astrocytes, respectively, and induced the conversion of M1 microglia and A1 astrocytes to M2 microglia and A2 astrocytes, respectively. In conclusion, daphnetin ameliorates NP by inhibiting the expression of inflammatory factors and chemokines and the polarization of glial cells in the spinal cord of NP rats. This study provides a theoretical basis for the treatment of NP with daphnetin to expand the clinical application of daphnetin.

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Section: Resultsmentioning

confidence: 99%

Daphnetin Improves Neuropathic Pain by Inhibiting the Expression of Chemokines and Inflammatory Factors in the Spinal Cord and Interfering with Glial Cell Polarization

et al. 2023

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“… Ruan, et al (2022) reported that LPS attack resulted in an imbalance in broiler intestinal homeostasis with changes in the levels of metabolites related to energy metabolism, including reduced concentrations of butyric acid, 3-hydroxybutyric acid, malic acid, and succinic acid, and increased levels of alanine. Zhao et al (2022) found that LPS produced 3 breakpoints in the TCA cycle of macrophages, namely, downregulation of isocitrate dehydrogenase, inhibition of succinate accumulation and SDH activity, and a significant decrease in the expression level of carboglutarate dehydrogenase and its substrate α-ketoglutarate. In our study, some key metabolites involved in the TCA cycle (NAD, acetyl CoA, citric acid, and pyruvic acid) were significantly down-regulated.…”

Section: Discussionmentioning

confidence: 98%

Molecular and metabolic responses to immune stress in the jejunum of broiler chickens: transcriptomic and metabolomic analysis

Hu,

Du,

Shao

et al. 2024

Poultry Science

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“…In addition, during the inflammatory phase, M1 microphages increase the production of tissue inhibitor of matrix metalloproteinase (TIMP) to inhibit ECM degradation ( Mahalanobish et al, 2020 ). However, M2 macrophages degrade ECM during the anti-inflammatory phase by secreting MMPs (i.e., MMP1, MMP12, MMP9), thus promoting fibrosis resolution ( Ramachandran et al, 2012 ; Zhao et al, 2022 ). Oxidative stress is a key event in pulmonary fibrosis due to inflammation.…”

Section: Immunometabolism Controls Immune Cells In Fibrosismentioning

confidence: 99%

Immunometabolism changes in fibrosis: from mechanisms to therapeutic strategies

et al. 2023

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Immune cells are essential for initiating and developing the fibrotic process by releasing cytokines and growth factors that activate fibroblasts and promote extracellular matrix deposition. Immunometabolism describes how metabolic alterations affect the function of immune cells and how inflammation and immune responses regulate systemic metabolism. The disturbed immune cell function and their interactions with other cells in the tissue microenvironment lead to the origin and advancement of fibrosis. Understanding the dysregulated metabolic alterations and interactions between fibroblasts and the immune cells is critical for providing new therapeutic targets for fibrosis. This review provides an overview of recent advances in the pathophysiology of fibrosis from the immunometabolism aspect, highlighting the altered metabolic pathways in critical immune cell populations and the impact of inflammation on fibroblast metabolism during the development of fibrosis. We also discuss how this knowledge could be leveraged to develop novel therapeutic strategies for treating fibrotic diseases.

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Grossamide attenuates inflammation by balancing macrophage polarization through metabolic reprogramming of macrophages in mice

Cited by 7 publications

References 50 publications

Daphnetin Improves Neuropathic Pain by Inhibiting the Expression of Chemokines and Inflammatory Factors in the Spinal Cord and Interfering with Glial Cell Polarization

Daphnetin Improves Neuropathic Pain by Inhibiting the Expression of Chemokines and Inflammatory Factors in the Spinal Cord and Interfering with Glial Cell Polarization

Molecular and metabolic responses to immune stress in the jejunum of broiler chickens: transcriptomic and metabolomic analysis

Immunometabolism changes in fibrosis: from mechanisms to therapeutic strategies

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