Ganoderma lucidum polysaccharides ameliorate lipopolysaccharide-induced acute pneumonia via inhibiting NRP1-mediated inflammation
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 × 106 (model) and 7.1 × 105 (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.
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.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2022 |
---|---|
Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:60 |
---|---|
Enthalten in: |
Pharmaceutical biology - 60(2022), 1 vom: 04. Dez., Seite 2201-2209 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Zhang, Xuelian [VerfasserIn] |
---|
Links: |
---|
Anmerkungen: |
Date Completed 16.11.2022 Date Revised 16.11.2022 published: Print Citation Status MEDLINE |
---|
doi: |
10.1080/13880209.2022.2142615 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM348874979 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM348874979 | ||
003 | DE-627 | ||
005 | 20231226041313.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231226s2022 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1080/13880209.2022.2142615 |2 doi | |
028 | 5 | 2 | |a pubmed24n1162.xml |
035 | |a (DE-627)NLM348874979 | ||
035 | |a (NLM)36373992 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Zhang, Xuelian |e verfasserin |4 aut | |
245 | 1 | 0 | |a Ganoderma lucidum polysaccharides ameliorate lipopolysaccharide-induced acute pneumonia via inhibiting NRP1-mediated inflammation |
264 | 1 | |c 2022 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 16.11.2022 | ||
500 | |a Date Revised 16.11.2022 | ||
500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a 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 | ||
520 | |a OBJECTIVE: To explore the protective role of GLP against LPS-induced acute pneumonia and investigate possible mechanisms | ||
520 | |a 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 | ||
520 | |a RESULTS: GLP suppressed inflammatory cell infiltration. In BALF, cell counts were 1.1 × 106 (model) and 7.1 × 105 (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 | ||
520 | |a 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 | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Randomized Controlled Trial, Veterinary | |
650 | 4 | |a COVID-19 | |
650 | 4 | |a Ganodermataceae | |
650 | 4 | |a anti-inflammatory | |
650 | 4 | |a pneumonocyte apoptosis | |
650 | 7 | |a Caspase 3 |2 NLM | |
650 | 7 | |a EC 3.4.22.- |2 NLM | |
650 | 7 | |a Interleukin-6 |2 NLM | |
650 | 7 | |a Lipopolysaccharides |2 NLM | |
650 | 7 | |a Neuropilin-1 |2 NLM | |
650 | 7 | |a 144713-63-3 |2 NLM | |
650 | 7 | |a Polysaccharides |2 NLM | |
700 | 1 | |a Wu, Daoshun |e verfasserin |4 aut | |
700 | 1 | |a Tian, Yu |e verfasserin |4 aut | |
700 | 1 | |a Chen, Xiangdong |e verfasserin |4 aut | |
700 | 1 | |a Lan, Jin |e verfasserin |4 aut | |
700 | 1 | |a Wei, Fei |e verfasserin |4 aut | |
700 | 1 | |a Li, Ye |e verfasserin |4 aut | |
700 | 1 | |a Luo, Yun |e verfasserin |4 aut | |
700 | 1 | |a Sun, Xiaobo |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Pharmaceutical biology |d 1997 |g 60(2022), 1 vom: 04. Dez., Seite 2201-2209 |w (DE-627)NLM097504416 |x 1744-5116 |7 nnns |
773 | 1 | 8 | |g volume:60 |g year:2022 |g number:1 |g day:04 |g month:12 |g pages:2201-2209 |
856 | 4 | 0 | |u http://dx.doi.org/10.1080/13880209.2022.2142615 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 60 |j 2022 |e 1 |b 04 |c 12 |h 2201-2209 |