Liensinine alleviates LPS-induced acute lung injury by blocking autophagic flux via PI3K/AKT/mTOR signaling pathway

Wang, Cheng; Zou, Kang; Diao, Yunlian; Zhou, Chaoqi; Zhou, Jia; Yang, Yuting; Zeng, Zhenguo

doi:10.1016/j.biopha.2023.115813

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…The PI3K/AKT pathway is another key pathway known to play a role in neuroprotection by decreasing the expression of proin ammatory cytokines and increasing the expression of anti-apoptotic factors [30].…”

Section: Discussionmentioning

confidence: 99%

Activation of cannabinoid receptor 2 inhibits LPS-induced neuroinflammation via PI3K/Akt signaling pathway in mice

Wang,

denghan,

Sui

et al. 2024

Preprint

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Parkinson's disease (PD) is a common neurodegenerative disease characterized by selective loss of dopaminergic neurons in the substantia nigra (SN) and neuroinflammation mediated by overactivated microglia and astrocytes. Cannabinoid receptor 2 (CB2R) is primarily present on peripheral immune cells and microglia, exerts a significant immunomodulatory effect. However, its antineuroinflammatory effects and the precise mechanism are still unclear. Therefore, this study attempts to investigate the effect of CB2R on neuroinflammation and the underlying mechanisms. Mice were injected with Lipopolysaccharide (LPS) into both sides of the SN using a stereotactic injection method to establish neuroinflammatory model. Pole test and rotarod test were performed to examine the ability of balance and motor coordination of mice. Immunohistochemistry (IHC) and immunofluorescence (IF) were performed on brain tissue sections to observe of tyrosine hydroxylase (TH), Iba1 and GFAP. RT-PCR was examined for inflammatory factors TNF-α, IL-6, IL-1β, iNOS and COX-2. The expression of PI3K/AKT signaling pathway-related proteins was examined by Western blot. Our studies showed that CB2R agonist (JWH133) protected dopaminergic neurons and improve motor dysfunction by inhibiting the activation of glial cells and the release of pro-inflammatory mediators in SN of mice induced by LPS. Furthermore, JWH133 also restored the phosphorylation of PI3K and Akt, which was downregulated by LPS in SN. However, CB2R knockout mice aggravated the loss of dopaminergic neurons and the decline of motor function. After CB2R knockout, the number of activated glial cells was significantly increased, and the expression of pro-inflammatory mediators was increased. The results suggested that activation of CB2R ameliorated LPS-induced neuroinflammation through the PI3K/Akt pathway.

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Section: Discussionmentioning

confidence: 99%

Activation of cannabinoid receptor 2 inhibits LPS-induced neuroinflammation via PI3K/Akt signaling pathway in mice

Wang,

denghan,

Sui

et al. 2024

Preprint

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“…and allowed to breathe normally during the procedure. [15] The ALI model was induced by intratracheal LPS administration, with MOOs administered intraperitoneally for 2 days as a preventive measure. Control mice received normal saline.…”

Section: Animal Experimentsmentioning

confidence: 99%

Ameliorative Effect of Morinda Officinalis Oligosaccharides on LPS‐Induced Acute Lung Injury

Qing,

Wu,

Liu

et al. 2024

Chemistry & Biodiversity

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Acute lung injury (ALI) is a disease characterized by extensive lung damage and rampant inflammation, with a high mortality rate and no effective treatments available. Morinda officinalis oligosaccharide (MOOs), derived from the root of the traditional Chinese medicinal herb Morinda officinalis, known for its immune‐boosting properties, presents a novel therapeutic possibility. To date, the impact of MOOs on ALI has not been explored. We discovered that MOOs significantly mitigated the pathological damage and decreased the expression of pro‐inflammatory cytokines in LPS‐induced ALI in mice. Complementary in vitro studies further demonstrated that MOOs effectively attenuated the M1 polarization induced by LPS. Network pharmacology analysis identified HSP90AA1, HSP90AB1, and NF‐κB as key overlapping targets within a protein‐protein interaction (PPI) network. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses elucidated the biological processes and signaling pathways implicated in MOOs' therapeutic action on ALI. Subsequently, molecular docking affirmed the binding of MOOs to the active sites of these identified targets. Collectively, these findings suggest that MOOs confer protection against ALI through a multi‐target, multi‐pathway mechanism, offering a promising new therapeutic strategy to mitigate this severe pulmonary condition.

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Chondrocyte autophagy mediated by T-2 toxin via AKT/TSC/Rheb/mTOR signaling pathway and protective effect of CSA-SeNP

Lin,

Liu,

Qiao

et al. 2024

Osteoarthritis and Cartilage

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Liensinine alleviates LPS-induced acute lung injury by blocking autophagic flux via PI3K/AKT/mTOR signaling pathway

Cited by 4 publications

References 33 publications

Activation of cannabinoid receptor 2 inhibits LPS-induced neuroinflammation via PI3K/Akt signaling pathway in mice

Activation of cannabinoid receptor 2 inhibits LPS-induced neuroinflammation via PI3K/Akt signaling pathway in mice

Ameliorative Effect of Morinda Officinalis Oligosaccharides on LPS‐Induced Acute Lung Injury

Chondrocyte autophagy mediated by T-2 toxin via AKT/TSC/Rheb/mTOR signaling pathway and protective effect of CSA-SeNP

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