Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
Pharm Biol. 2022 Dec;60(1):2201-2209. doi: 10.1080/13880209.2022.2142615.
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.
To explore the protective role of GLP against LPS-induced acute pneumonia and investigate possible mechanisms.
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.
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-α 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.
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.
从灵芝（Leyss. ex Fr.）Karst.（灵芝科）中提取的多糖（GLP）具有抗炎作用，包括抗神经炎症和抗结肠炎。然而，GLP 在急性肺炎中的作用尚不清楚。
探讨 GLP 对脂多糖（LPS）诱导的急性肺炎的保护作用及其可能的机制。
GLP 经酸水解和 PMP 衍生化后，采用高效液相色谱（HPLC）进行分析提取。将 60 只 C57BL/6N 雄性小鼠随机分为 6 组：假手术组、模型组、LPS+GLP（25、50 和 100mg/kg/d 灌胃 2 周）和 LPS+地塞米松（6mg/kg/d 腹腔注射 1 周）组。通过气管内注射 LPS 建立急性肺炎小鼠模型。苏木精和伊红（H&E）染色评估肺损伤。酶联免疫吸附试验（ELISA）和实时定量 PCR 用于评估炎症因子的表达。Western blot 用于测量 Neuropilin-1 表达以及与凋亡和自噬相关的蛋白质。
GLP 抑制炎症细胞浸润。在 BALF 中，细胞计数为 1.1×10（模型）和 7.1×10（100mg/kg）。GLP（25、50 和 100mg/kg）治疗可降低 GM-CSF 和 IL-6 的释放。IL-1β、IL-6、TNF-α和 Saa3 基因的表达减少。GLP 治疗还抑制了 Neuropilin-1（NRP1）的激活，上调了 Bcl2/Bax 和 LC3 的水平，并导致 C-Caspase 3/Caspase 3 比值和 P62 表达下调。
GLP 可通过多种机制保护 LPS 诱导的急性肺炎：阻止炎症细胞浸润、抑制细胞因子分泌、抑制 NRP1 激活以及调节肺细胞凋亡和自噬。
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