Anti-Inflammatory Activity of Sanghuangporus sanghuang Mycelium

Int J Mol Sci. 2017 Feb 7;18(2):347. doi: 10.3390/ijms18020347.

Abstract

Acute lung injury (ALI) is characterized by inflammation of the lung tissue and oxidative injury caused by excessive accumulation of reactive oxygen species. Studies have suggested that anti-inflammatory or antioxidant agents could be used for the treatment of ALI with a good outcome. Therefore, our study aimed to test whether the mycelium extract of Sanghuangporus sanghuang (SS-1), believed to exhibit antioxidant and anti-inflammatory properties, could be used against the excessive inflammatory response associated with lipopolysaccharides (LPS)-induced ALI in mice and to investigate its possible mechanism of action. The experimental results showed that the administration of SS-1 could inhibit LPS-induced inflammation. SS-1 could reduce the number of inflammatory cells, inhibit myeloperoxidase (MPO) activity, regulate the TLR4/PI3K/Akt/mTOR pathway and the signal transduction of NF-κB and MAPK pathways in the lung tissue, and inhibit high mobility group box-1 protein 1 (HNGB1) activity in BALF. In addition, SS-1 could affect the synthesis of antioxidant enzymes Heme oxygenase 1 (HO-1) and Thioredoxin-1 (Trx-1) in the lung tissue and regulate signal transduction in the KRAB-associated protein-1 (KAP1)/nuclear factor erythroid-2-related factor Nrf2/Kelch Like ECH associated Protein 1 (Keap1) pathway. Histological results showed that administration of SS-1 prior to induction could inhibit the large-scale LPS-induced neutrophil infiltration of the lung tissue. Therefore, based on all experimental results, we propose that SS-1 exhibits a protective effect against LPS-induced ALI in mice. The mycelium of S. sanghuang can potentially be used for the treatment or prevention of inflammation-related diseases.

Keywords: HNGB; HO-1; KAP1/Nrf2 pathway; PI3K/Akt/mTOR pathways; acute lung injury; lipopolysaccharide; mycelium of Sanghuangporus sanghuang.

MeSH terms

  • Acute Lung Injury / drug therapy
  • Acute Lung Injury / etiology
  • Acute Lung Injury / metabolism*
  • Acute Lung Injury / pathology*
  • Animals
  • Anti-Inflammatory Agents / administration & dosage
  • Anti-Inflammatory Agents / chemistry
  • Anti-Inflammatory Agents / pharmacology*
  • Basidiomycota / chemistry*
  • Biological Products / administration & dosage
  • Biological Products / chemistry
  • Biological Products / pharmacology*
  • Cytokines / metabolism
  • Disease Models, Animal
  • Heme Oxygenase-1 / metabolism
  • Inflammation Mediators / metabolism
  • Lipopolysaccharides / adverse effects
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / metabolism
  • Male
  • Mice
  • Mitogen-Activated Protein Kinases / metabolism
  • Mycelium / chemistry*
  • NF-E2-Related Factor 2 / metabolism
  • NF-kappa B / metabolism
  • Nitric Oxide / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt
  • Signal Transduction / drug effects
  • TOR Serine-Threonine Kinases / metabolism
  • Thioredoxins / metabolism
  • Toll-Like Receptor 4 / metabolism

Substances

  • Anti-Inflammatory Agents
  • Biological Products
  • Cytokines
  • Inflammation Mediators
  • Lipopolysaccharides
  • NF-E2-Related Factor 2
  • NF-kappa B
  • Toll-Like Receptor 4
  • Nitric Oxide
  • Thioredoxins
  • Heme Oxygenase-1
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • Mitogen-Activated Protein Kinases