In vitro Synthesis of a Recombinant Fungal Immunomodulatory Protein from Lingzhi or Reishi Medicinal Mushroom, Ganoderma lucidum (W.Curt.:Fr.) P.Karst. (Aphyllophoromycetideae) and Analysis of Its Immunomodulatory Activity

2010 ◽  
Vol 12 (4) ◽  
pp. 347-358 ◽  
Author(s):  
Qi-zhang Li ◽  
Xue-fei Wang ◽  
Ting-wen Bao ◽  
Liang Ran ◽  
Juan Lin ◽  
...  
Keyword(s):  
Ganoderma Lucidum ◽  
Immunomodulatory Activity ◽  
Medicinal Mushroom ◽  
In Vitro Synthesis ◽  
Fungal Immunomodulatory Protein ◽  
Immunomodulatory Protein

scholarly journals Immunomodulatory activity of Ganoderma lucidum immunomodulatory protein via PI3K/Akt and MAPK signaling pathways in macrophage RAW264.7 cells

2018 ◽  
Author(s):  
Xuanwei Zhou ◽  
Qizhang Li ◽  
Yuzhou Chang ◽  
Liu-Ding-Ji Li ◽  
Xiaoyu Du ◽  
...  
Keyword(s):  
Ganoderma Lucidum ◽  
Kinase Inhibitor ◽  
Mapk Signaling ◽  
Raw264.7 Cells ◽  
In Vitro Assays ◽  
Immunomodulatory Activity ◽  
Inos Mrna ◽  
Sequencing Analysis ◽  
Mrna Levels ◽  
Immunomodulatory Protein

Ganoderma lucidum, a traditional edible and medicinal fungus, holds an important status in health care systems in China and other Asian countries. Fungal immunomodulatory protein (FIP), one of the active ingredients isolated from G. lucidum, is a class of naturally occurring proteins and possesses potential biological functions. This study was conducted to explore the molecular mechanism of its immunomodulatory potency in immune responses of macrophages. In vitro assays of biological activity indicated that rFIP-glu significantly activated macrophage RAW264.7 cells, and possessed the ability of pro- and anti-inflammation the cells. RNA sequencing analysis showed that macrophage activation involved Toll-like receptors and mitogen-activated protein kinases pathways. Furthermore, qRT-PCR indicated that phosphoinositide 3 kinase inhibitor LY294002 blocked the mRNA levels of MCP-1, MEK1/2 inhibitor U0126 reduced the mRNA levels of TNF-α and MCP-1, and JNK inhibitor SP600125 prevented the up-regulation of iNOS mRNA in the rFIP-glu-induced cells. FIP-glu mediated these inflammatory effects not through a general pathway, instead through a different pathway for different inflammatory mediator. These data indicate the possibility that rFIP-glu has an important immune-regulation function and thus has potential therapeutic uses.

Immunomodulatory activity of Ganoderma lucidum immunomodulatory protein via PI3K/Akt and MAPK signaling pathways in RAW264.7 cells

2019 ◽  
Vol 234 (12) ◽  
pp. 23337-23348 ◽  
Author(s):  
Qi‐Zhang Li ◽  
Yu‐Zhou Chang ◽  
Zhu‐Mei He ◽  
Lei Chen ◽  
Xuan‐Wei Zhou
Keyword(s):  
Signaling Pathways ◽  
Ganoderma Lucidum ◽  
Mapk Signaling ◽  
Raw264.7 Cells ◽  
Immunomodulatory Activity ◽  
Immunomodulatory Protein ◽  
Mapk Signaling Pathways

scholarly journals Anti-inflammatory and Neuroprotective Effects of Fungal Immunomodulatory Protein Involving Microglial Inhibition

2018 ◽  
Vol 19 (11) ◽  
pp. 3678 ◽  
Author(s):  
Wen-Ying Chen ◽  
Cheng-Yi Chang ◽  
Jian-Ri Li ◽  
Jiaan-Der Wang ◽  
Chih-Cheng Wu ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Tyrosine Phosphatase ◽  
Primary Cultures ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuroprotective Effects ◽  
Fungal Immunomodulatory Protein ◽  
Immunomodulatory Protein ◽  
Anti Inflammatory

Microglia polarization of classical activation state is crucial to the induction of neuroinflammation, and has been implicated in the pathogenesis of numerous neurodegenerative diseases. Fungal immunomodulatory proteins are emerging health-promoting natural substances with multiple pharmacological activities, including immunomodulation. Herein, we investigated the anti-inflammatory and neuroprotective potential of fungal immunomodulatory protein extracted from Ganoderma microsporum (GMI) in an in vitro rodent model of primary cultures. Using primary neuron/glia cultures consisting of neurons, astrocytes, and microglia, a GMI showed an alleviating effect on lipopolysaccharide (LPS)/interferon-γ (IFN-γ)-induced inflammatory mediator production and neuronal cell death. The events of neuroprotection caused by GMI were accompanied by the suppression of Nitric Oxide (NO), Tumor Necrosis Factor-α (TNF-α), Interleukin-1β (IL-1β), and Prostaglandin E2 (PGE2) production, along with the inhibition of microglia activation. Mechanistic studies showed that the suppression of microglia pro-inflammatory polarization by GMI was accompanied by the resolution of oxidative stress, the preservation of protein tyrosine phosphatase and serine/threonine phosphatase activity, and the reduction of NF-κB, AP-1, cyclic AMP response element-binding protein (CREB), along with signal transducers and activators of transcription (Stat1) transcriptional activities and associated upstream activators. These findings suggest that GMI may have considerable potential towards the treatment of neuroinflammation-mediated neurodegenerative diseases.

scholarly journals Effect of Trovafloxacin on Production of Cytokines by Human Monocytes

1998 ◽  
Vol 42 (7) ◽  
pp. 1713-1717 ◽  
Author(s):  
Anis A. Khan ◽  
Teri R. Slifer ◽  
Jack S. Remington
Keyword(s):  
Inflammatory Responses ◽  
Immunomodulatory Activity ◽  
Human Monocytes ◽  
Healthy Human ◽  
Necrosis Factor Alpha ◽  
In Vitro Synthesis ◽  
Cytokine Synthesis ◽  
Diphenyl Tetrazolium Bromide

ABSTRACT Antibiotics have previously been shown to have immunomodulatory effects. We examined the effect of the broad-spectrum fluoroquinoline antibiotic trovafloxacin on cytokine synthesis by monocytes obtained from healthy human volunteers and stimulated with either lipopolysaccharide or gram-positive cells (heat-killedStaphylococcus aureus [Pansorbin]). Trovafloxacin levels achievable in humans suppressed in vitro synthesis of each of the cytokines analyzed, viz., interleukin-1α (IL-1α), IL-1β, IL-6, IL-10, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha. This effect was not due to direct effects of the drug on cellular viability; at these concentrations, trovafloxacin did not have demonstrable cytotoxicity for the monocytes, as determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. Although similar patterns of suppression of cytokine synthesis were observed in samples obtained from the same volunteers on different days, there were significant day-to-day variations. These results reveal that trovafloxacin possesses significant immunomodulatory activity in vitro and suggest that suppression of acute-phase inflammatory responses may occur in vivo, elicited through trovafloxacin’s effect on cytokine synthesis by human monocytes.

scholarly journals Inhibitive activity of medicinal mushroom Ganoderma lucidum on colorectal cancer by attenuating inflammation

2021 ◽  
Author(s):  
Mandy M Liu ◽  
Tiantian Liu ◽  
Steven Yeung ◽  
Zhijun Wang ◽  
Bradley Andresen ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Ganoderma Lucidum ◽  
Gene Networks ◽  
Enrichment Analysis ◽  
Pathway Enrichment Analysis ◽  
Medicinal Mushroom ◽  
Hek 293 ◽  
Multiple Tumor ◽  
Normal Tissues

Abstract The medicinal mushroom Ganoderma lucidum (GL, Reishi or Lingzhi) exhibits inhibitive effect on cancers. However, the underline mechanism of the antitumor activity of GL is still not fully understood. In this study, we characterized the gene networks regulated by a commercial product of GL containing mixture of spore and fruiting body, namely “GLSF”, in colorectal carcinoma. We found that, in vitro co-administration of GLSF extract at non-toxic concentrations significantly potentiated growth inhibition and apoptosis induced by paclitaxel in CT26 and HCT-15 cells. GLSF inhibited NF-κB promoter activity in HEK-293 cells but did not affect the function of P-glycoprotein in K562/DOX cells. Furthermore, we found that when mice were fed with a modified diet containing GLSF for one month prior to the CT26 tumor cell inoculation, GLSF alone or combined with Nab-paclitaxel markedly suppressed tumor growth and induced apoptosis. RNA-seq analysis of tumor tissues derived from GLSF-treated mice identified 53 differentially expressed genes compared to normal tissues. Many of GLSF-downregulated genes were involved in NF-κB-regulated inflammation pathways, such as IL-1β, IL-11 and Cox-2. Pathway enrichment analysis suggested several inflammatory pathways involving leukocyte migration and adhesion were most affected by the treatment. Upstream analysis predicted activation of multiple tumor suppressors such as α-catenin and TP53 and inhibition of critical inflammatory mediators. “Cancer” was the major significantly inhibited biological effect due to GLSF treatment. These results demonstrate that GLSF can improve the therapeutic outcome for colorectal cancer through a mechanism involving suppressing NF-κB-regulated inflammation and carcinogenesis.

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