Propofol promotes migration, alleviates inflammation, and apoptosis of lipopolysaccharide‐induced human pulmonary microvascular endothelial cells by activating <scp>PI3K</scp>/<scp>AKT</scp> signaling pathway via upregulating <scp>APOM</scp> expression

Wang, Li; Tang, Xingming; Li, Shuping

doi:10.1002/ddr.21869

Cited by 13 publications

(3 citation statements)

References 33 publications

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“…In a previous study by the authors, KEGG pathway enrichment analysis revealed that the PI3K/AKT signalling pathway was the main signalling pathway for gene enrichment in lung tissues after PQ poisoning and AH 2 QdS treatment (26). The PI3K/AKT signalling pathway is important in the regulation of cell survival as well as repairing endothelial damage (43)(44)(45)(46)(47).…”

Section: Discussionmentioning

confidence: 99%

Anthrahydroquinone‑2,6‑disulfonate attenuates PQ‑induced acute lung injury through decreasing pulmonary microvascular permeability via inhibition of the PI3K/AKT/eNOS pathway

Li,

Yi,

Chen

et al. 2024

Int J Mol Med

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Section: Discussionmentioning

confidence: 99%

Anthrahydroquinone‑2,6‑disulfonate attenuates PQ‑induced acute lung injury through decreasing pulmonary microvascular permeability via inhibition of the PI3K/AKT/eNOS pathway

Li,

Yi,

Chen

et al. 2024

Int J Mol Med

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“…The PI3K/Akt signaling pathway can promote cell survival and growth in several ways, including the suppression of inflammation and the regulation of apoptosis and ERS. 27 For example, PI3K/Akt downregulates pro-apoptotic proteins including Bad, BAX, and caspase. 28 The regulation of apoptosis to protect against lung injury is also mediated by the activation of PI3K/Akt signaling.…”

Section: Discussionmentioning

confidence: 99%

Penehyclidine hydrochloride protects against lipopolysaccharide-induced acute lung injury by promoting the PI3K/Akt pathway

Weng

Liu

Shi

et al. 2023

Int J Immunopathol Pharmacol

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Introduction Acute lung injury (ALI) attracted attention among physicians because of its high mortality. We aimed to determine whether the phosphatidylinositol-3 kinase (PI3K)/protein kinase B (Akt) pathway is involved in the protective effects of penehyclidine hydrochloride (PHC) against lipopolysaccharide (LPS)-induced ALI. Methods H&E staining was used to observed pathological changes in the lung tissues. ELISA was used to evaluate the concentration of inflammatory mediators in the bronchoalveolar lavage fluid (BALF). White-light microscopy was performed to observe the TUNEL-positive nuclei. The viability of NR8383 alveolar macrophages was determined by using CCK-8. The levels of MPO, MDA, SOD, and GSH-Px were analyzed using ELISA kits. Western blotting was used to evaluate the ERS-associated protein levels and the phosphorylation of PI3K and Akt. Results PHC administration defended against LPS-induced histopathological deterioration and increased pulmonary edema and lung injury scores, while all of these beneficial effects were inhibited by LY. In addition, PHC administration mitigated oxidative stress as indicated by decreases in lung myeloperoxidase (MPO) and malondialdehyde (MDA) concentrations, and increases in glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) concentrations. It also alleviated LPS-induced inflammation. PHC administration attenuated apoptosis-associated protein levels, improved cell viability, and decreased the number of TdT-mediated dUTP Nick-End Labeling (TUNEL)-positive cells. Furthermore, PHC inhibited ERS-associated protein levels. Meanwhile, the protection of PHC against inflammation, oxidative stress, apoptosis, and ERS was inhibited by LY. Moreover, PHC administration increased PI3K and Akt phosphorylation, indicating that the upregulation of the PI3K/Akt pathway, while this pathway was inhibited by LY. Conclusion PHC significantly activates the PI3K/Akt pathway to ameliorate the extent of damage to pulmonary tissue, inflammation, oxidative stress, apoptosis, and ERS in LPS-induced ALI.

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“…First of all, SREBF1, as the central transcription factor regulating lipid metabolism, mainly regulates the expression of the factors required for fatty acid synthesis ( 30 ), which has recently been proved to be the reason why PI3K-AKT-mTOR signaling pathway endows cancer cells with the ability to resist iron death ( 31 ). Furthermore, ApoM is closely related to the AKT-mTOR signaling pathway and is associated with inflammation, apoptosis and insulin resistance ( 11 , 32 , 33 ). Future work will aim to prove that ApoM affects SREBF1 through certain pathways (at least the PI3K-AKT-mTOR signaling pathway).…”

Section: Discussionmentioning

confidence: 99%

ApoM regulates PFKL through the transcription factor SREBF1 to inhibit the proliferation, migration and metastasis of liver cancer cells

et al. 2022

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Apolipoprotein M (ApoM) is considered a protective factor that inhibits the occurrence and development of liver cancer, but the specific underlying mechanisms require further investigation. Previous studies have demonstrated that ApoM gene knockout promotes the expression of the transcription factor sterol regulatory element-binding protein 1 (SREBP1; also known as SREBF1) in the livers of mice. SREBF1 is closely associated with factors involved in fatty acid synthesis and has a role in the promotion of tumor progression. The present study initially confirmed that the expression levels of ApoM in cancer tissues were significantly decreased compared with those in normal tissue, while the expression levels of SREBF1 were significantly increased. In addition, ApoM gene knockout significantly increased the expression levels of SREBF1 and the key glycolytic enzyme ATP-dependent 6-phosphofructokinase, liver type (PFKL). Binding site prediction and a dual-luciferase reporter gene assay indicated that SREBF1 regulates the promoter region of PFKL. To the best of our knowledge, the present study was the first to propose the regulation of glycolytic enzyme transcription levels by SREBF1. Furthermore, cell proliferation and Transwell assays demonstrated that ApoM gene knockout increased the expression levels of SREBF1 and further enhanced the activity of the promoter region of PFKL, ultimately promoting the proliferation, migration and invasion of liver cancer cells.

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Propofol promotes migration, alleviates inflammation, and apoptosis of lipopolysaccharide‐induced human pulmonary microvascular endothelial cells by activating PI3K/AKT signaling pathway via upregulating APOM expression

Cited by 13 publications

References 33 publications

Anthrahydroquinone‑2,6‑disulfonate attenuates PQ‑induced acute lung injury through decreasing pulmonary microvascular permeability via inhibition of the PI3K/AKT/eNOS pathway

Anthrahydroquinone‑2,6‑disulfonate attenuates PQ‑induced acute lung injury through decreasing pulmonary microvascular permeability via inhibition of the PI3K/AKT/eNOS pathway

Penehyclidine hydrochloride protects against lipopolysaccharide-induced acute lung injury by promoting the PI3K/Akt pathway

ApoM regulates PFKL through the transcription factor SREBF1 to inhibit the proliferation, migration and metastasis of liver cancer cells

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