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Article Publish Status: FREE
Abstract Title:

polysaccharides ameliorate lipopolysaccharide-induced acute pneumonia via inhibiting NRP1-mediated inflammation.

Abstract Source:

Pharm Biol. 2022 Dec ;60(1):2201-2209. PMID: 36373992

Abstract Author(s):

Xuelian Zhang, Daoshun Wu, Yu Tian, Xiangdong Chen, Jin Lan, Fei Wei, Ye Li, Yun Luo, Xiaobo Sun

Article Affiliation:

Xuelian Zhang

Abstract:

CONTEXT: polysaccharides (GLP), from(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 × 10(model) and 7.1 × 10(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-1β, IL-6, TNF-αand 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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