Ganoderma lucidum polysaccharides ameliorated depression-like behaviors in the chronic social defeat stress depression model via modulation of Dectin-1 and the innate immune system

Li, Haoran; Xiao, Yuhuan; Liang, Han; Jia, Yanjie; Luo, Shaolei; Zhang, Dandan; Zhang, Ling; Wu, Peng; Xiao, Chunjie; Kan, Weijing; Du, Jing; Bao, Hongkun

doi:10.1016/j.brainresbull.2021.03.002

Cited by 34 publications

(24 citation statements)

References 47 publications

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“…Laminarin, a water-soluble β -glucan is a dectin-1 antagonist that binds to dectin-1 without stimulating downstream signaling. [ 46 , 47 ] Twenty-eight days after mice were put on an ethanol diet, they were treated with laminarin (300 mg kg −1 of body weight), brain tissue lysates and the supernatants extracted from brain tissue of treated mice were analyzed. The results indicate that the alcohol stimulated activation of NF- κ B, Syk, and induction of TNF α compared with results from mice fed the control liquid diet.…”

Section: Resultsmentioning

confidence: 99%

Restoring Oat Nanoparticles Mediated Brain Memory Function of Mice Fed Alcohol by Sorting Inflammatory Dectin‐1 Complex Into Microglial Exosomes

Teng

et al. 2021

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Microglia modulate pro‐inflammatory and neurotoxic activities. Edible plant‐derived factors improve brain function. Current knowledge of the molecular interactions between edible plant‐derived factors and the microglial cell is limited. Here an alcohol‐induced chronic brain inflammation model is used to identify that the microglial cell is the novel target of oat nanoparticles (oatN). Oral administration of oatN inhibits brain inflammation and improves brain memory function of mice that are fed alcohol. Mechanistically, ethanol activates dectin‐1 mediated inflammatory pathway. OatN is taken up by microglial cells via β‐glucan mediated binding to microglial hippocalcin (HPCA) whereas oatN digalactosyldiacylglycerol (DGDG) prevents assess of oatN β‐glucan to dectin‐1. Subsequently endocytosed β‐glucan/HPCA is recruited in an endosomal recycling compartment (ERC) via interaction with Rab11a. This complex then sequesters the dectin‐1 in the ERC in an oatN β‐glucan dependent manner and alters the location of dectin‐1 from Golgi to early endosomes and lysosomes and increases exportation of dectin‐1 into exosomes in an Rab11a dependent manner. Collectively, these cascading actions lead to preventing the activation of the alcoholic induced brain inflammation signing pathway(s). This coordinated assembling of the HPCA/Rab11a/dectin‐1 complex by oral administration of oatN may contribute to the prevention of brain inflammation.

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Section: Resultsmentioning

confidence: 99%

Restoring Oat Nanoparticles Mediated Brain Memory Function of Mice Fed Alcohol by Sorting Inflammatory Dectin‐1 Complex Into Microglial Exosomes

Teng

et al. 2021

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“…In patients with MS and in models of demyelination, CNS inflammation homoeostasis is destabilized by a variety of mechanisms [ 50 ]. Our previous studies showed that both Ganoderma lucidum polysaccharides and proteo- β -glucan from maitake exert their anti-inflammatory effects through the modulation of dectin-1 [ 32 , 51 ]. Therefore, this study confirmed that LNT, like other polysaccharides containing β -glucan, also mediated the anti-inflammatory effect through the modulation of dectin-1.…”

Section: Discussionmentioning

confidence: 99%

The Dectin-1 Receptor Signaling Pathway Mediates the Remyelination Effect of Lentinan through Suppression of Neuroinflammation and Conversion of Microglia

Zhang

Jia

Sun

et al. 2022

Journal of Immunology Research

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Demyelinating diseases such as multiple sclerosis (MS) are chronic inflammatory autoimmune diseases and involve demyelination and axonal degeneration. Microglia rapidly respond to changes in the environment by altering morphotype and function during the progressive disease stage. Although substantial progress has been made in the drug development for MS, treatment of the progressive forms of the disease remains unsatisfactory. There is great interest in identifying novel agents for treating MS. Lentinus edodes is a traditional food, which can improve physiological function. Lentinan (LNT), a type of polysaccharide extracted from mushroom Lentinus edodes, is an anti-inflammatory and immunomodulatory agent. Here, we studied the remyelination effects of LNT and its therapeutic target in regulating the functions of neuroinflammation. We found that LNT enhanced remyelination and rescued motor deficiency by regulating dectin-1 receptor to inhibit neuroinflammation and microglial cell transformation. LNT promoted the conversion of microglial cells from the M1 status induced by LPS to the M2 status, enhanced the anti-inflammatory markers IL-10 and BDNF, inhibited inflammatory markers TNF-α and IL-1β, and downregulated the microglia activation and oligodendrocyte and astrocyte proliferation by modulating dectin-1. If we injected the dectin-1-specific inhibitor laminarin (Lam), the remyelination effects induced by LNT were completely abolished. Thus, these results suggest that LNT is a novel and potential therapeutic agent that can rescue MS neuroimmune imbalance and remyelination through a dectin-1 receptor-dependent mechanism.

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“…The activity of MMP-9 could also be inhibited by GLPP in a dose-dependent manner [ 44 ]. Moreover, GLP significantly down-regulated pro-inflammatory cytokines, including iNOS, IL-1, and TNF-α, in a dose-dependent manner and up-regulated the anti-inflammation cytokine IL-10 in vivo and in vitro [ 45 , 46 ]. These effects produced by GLP in other inflammatory diseases caused by disorders of the immune system can also be observed in the treatment of RA.…”

Section: Inhibition Of Glp On Synovial Joint Inflammationmentioning

confidence: 99%

Potential Anti-Rheumatoid Arthritis Activities and Mechanisms of Ganoderma lucidum Polysaccharides

Meng

Yao

Zhang³

et al. 2023

Molecules

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Rheumatoid arthritis (RA) is a chronic and autoimmune disease characterized by inflammation, autoimmune dysfunction, and cartilage and bone destruction. In this review, we summarized the available reports on the protective effects of Ganoderma lucidum polysaccharides (GLP) on RA in terms of anti-inflammatory, immunomodulatory, anti-angiogenic and osteoprotective effects. Firstly, GLP inhibits RA synovial fibroblast (RASF) proliferation and migration, modulates pro- and anti-inflammatory cytokines and reduces synovial inflammation. Secondly, GLP regulates the proliferation and differentiation of antigen-presenting cells such as dendritic cells, inhibits phagocytosis by mononuclear macrophages and nature killer (NK) cells and regulates the ratio of M1, M2 and related inflammatory cytokines. In addition, GLP produced activities in balancing humoral and cellular immunity, such as regulating immunoglobulin production, modulating T and B lymphocyte proliferative responses and cytokine release, exhibiting immunomodulatory effects. Thirdly, GLP inhibits angiogenesis through the direct inhibition of vascular endothelial cell proliferation and induction of cell death and the indirect inhibition of vascular endothelial growth factor (VEGF) production in the cells. Finally, GLP can inhibit the production of matrix metalloproteinases and promote osteoblast formation, exerting protective effects on bone and articular cartilage. It is suggested that GLP may be a promising agent for the treatment of RA.

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Ganoderma lucidum polysaccharides ameliorated depression-like behaviors in the chronic social defeat stress depression model via modulation of Dectin-1 and the innate immune system

Cited by 34 publications

References 47 publications

Restoring Oat Nanoparticles Mediated Brain Memory Function of Mice Fed Alcohol by Sorting Inflammatory Dectin‐1 Complex Into Microglial Exosomes

Restoring Oat Nanoparticles Mediated Brain Memory Function of Mice Fed Alcohol by Sorting Inflammatory Dectin‐1 Complex Into Microglial Exosomes

The Dectin-1 Receptor Signaling Pathway Mediates the Remyelination Effect of Lentinan through Suppression of Neuroinflammation and Conversion of Microglia

Potential Anti-Rheumatoid Arthritis Activities and Mechanisms of Ganoderma lucidum Polysaccharides

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