期刊
PHARMACEUTICAL BIOLOGY
卷 60, 期 1, 页码 2201-2209出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/13880209.2022.2142615
关键词
Ganodermataceae; COVID-19; pneumonocyte apoptosis; anti-inflammatory
资金
- National Key Research and Development Plan Program [2019YFC1710504]
- CAMS Innovation Fund for Medical Sciences (CIFMS) Grant [2021-I2M-1-031]
The study found that Ganoderma lucidum polysaccharides (GLP) have a protective role in LPS-induced acute pneumonia. GLP acts through multiple mechanisms, including blocking inflammatory cell infiltration, inhibiting cytokine secretion, suppressing Neuropilin-1 (NRP1) activation, and regulating pneumonocyte apoptosis and autophagy.
Context Ganoderma lucidum polysaccharides (GLP), from Ganoderma lucidum (Leyss. ex Fr.) Karst. (Ganodermataceae), are reported to have anti-inflammatory effects, including anti-neuroinflammation and anti-colitis. Nevertheless, the role of GLP in acute pneumonia is unknown. Objective To explore the protective role of GLP against LPS-induced acute pneumonia and investigate possible mechanisms. Materials and methods GLP were extracted and used for high-performance liquid chromatography (HPLC) analysis after acid hydrolysis and PMP derivatization. Sixty C57BL/6N male mice were randomly divided into six groups: Sham, Model, LPS + GLP (25, 50 and 100 mg/kg/d administered intragastrically for two weeks) and LPS + dexamethasone (6 mg/kg/d injected intraperitoneally for one week). Acute pneumonia mouse models were established by intratracheal injection of LPS. Haematoxylin and eosin (H&E) staining was examined to evaluate lung lesions. ELISA and quantitative real-time PCR were employed to assess inflammatory factors expression. Western blots were carried out to measure Neuropilin-1 expression and proteins related to apoptosis and autophagy. Results GLP suppressed inflammatory cell infiltration. In BALF, cell counts were 1.1 x 10(6) (model) and 7.1 x 10(5) (100 mg/kg). Release of GM-CSF and IL-6 was reduced with GLP (25, 50 and 100 mg/kg) treatment. The expression of genes IL-1 beta, IL-6, TNF-alpha and Saa3 was reduced. GLP treatment also suppressed the activation of Neuropilin-1 (NRP1), upregulated the levels of Bcl2/Bax and LC3 and led to downregulation of the ratio C-Caspase 3/Caspase 3 and P62 expression. Discussion and conclusions GLP could protect against LPS-induced acute pneumonia through multiple mechanisms: blocking the infiltration of inflammatory cells, inhibiting cytokine secretion, suppressing NRP1 activation and regulating pneumonocyte apoptosis and autophagy.
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