Protective effect of triterpenes of Ganoderma lucidum on lipopolysaccharide-induced inflammatory responses and acute liver injury
| Autor: | Shuixing Yu, Ruiping Du, Zhongpeng Hu, Chao-Mei Ma, Haochi Zhang, Lei Xiu, Naoto Sato, Masao Hattori, Yanchen Liang, Ziyao Bian, Xiao Wang |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Lipopolysaccharides Reishi Lipopolysaccharide Cell Survival MAP Kinase Signaling System p38 mitogen-activated protein kinases Immunology Inflammation Pharmacology Protective Agents Biochemistry Cell Line 03 medical and health sciences chemistry.chemical_compound Lanosterol 0302 clinical medicine In vivo medicine Immunology and Allergy Animals Molecular Biology Liver injury Mice Inbred BALB C Molecular Structure Chemistry Macrophages NF-kappa B NF-κB Hematology medicine.disease Triterpenes 030104 developmental biology 030220 oncology & carcinogenesis TLR4 Cytokines Female medicine.symptom Chemical and Drug Induced Liver Injury |
| Zdroj: | Cytokine. 127 |
| ISSN: | 1096-0023 |
| Popis: | Ganoderma lucidum is a popular medicinal mushroom, which has been used as therapeutic for centuries in traditional Chinese medicine. Although G. lucidum showed strong protective effects in prevention or treatment of a variety of inflammatory diseases, the mechanisms underlying the anti-inflammatory properties of triterpenes of G. lucidum remain undefined. In the current study, we demonstrated that ethanol extract and triterpenes of G. lucidum specifically suppressed LPS-mediated inflammatory responses. Notably, ganodermanontriol inhibited the expressions and interactions of TLR4 and MyD88, NF-κB translocation to nucleus and its DNA binding activity, phosphorylation of p38, ErK1/2 and JNK. In vivo, we showed that ganodermanontriol effectively prevented LPS/D-Galactosamine-induced liver injury by reducing TNF-α and IL-6 production, and decrease of ALT/AST release. Collectively, our results revealed a novel role in inhibition of inflammatory diseases for triterpenes that may act through potential inhibition of TLR4-MyD88-mediated NF-κB and MAPK signaling pathways. |
| Databáze: | OpenAIRE |
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