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Protective Effect of the Total Alkaloid Extract from Bulbus on Cigarette Smoke-induced Beas-2B Cell Injury Model and Transcriptomic Analysis

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Journal Food Nutr Res
Date 2024 Jul 8
PMID 38974914
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Abstract

Background: Bulbus (BFP) is a traditional Chinese medicine that has long been used to treat lung diseases, but the active components and mechanism are still unclear.

Objective: This study aimed to investigate the effect and mechanism of the total alkaloid extract from BFP (BFP-TA) on cigarette smoke extract (CSE)-induced Beas-2B cells injury.

Design: The Beas-2B cells injury model was induced by 2% CSE, then the effect of BFP-TA on the levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD) and malondialdehyde (MDA) was detected according to the instructions of the T-AOC assay kit, the SOD detection kit and the MDA detection kit, and the production of ROS was detected by fluorescence microscopy. The effect of BFP-TA on Beas-2B cells apoptosis was detected by flow cytometry, and the effect of BFP-TA on related protein expression was detected by western blot. Subsequently, the effect of BFP-TA on differentially expressed genes (DEGs) in CSE-induced Beas-2B cells was studied by transcriptomic sequencing, and the expression of DEGs was verified by quantitative real-time polymerase chain reaction (qPCR).

Results: The results showed that BFP-TA could attenuate CSE-induced oxidative damage in Beas-2B cells by elevating T-AOC and SOD levels while inhibiting ROS and MDA levels, and the mechanism was potentially related to the SIRT1/Nrf2/Keap1 signaling pathway. Furthermore, BFP-TA could inhibit CSE-induced apoptosis by inhibiting the protein expression of Bax, MST1 and FOXO3a, and exert anti-inflammatory effect by inhibiting the activation of MAPK signaling pathway. Subsequently, transcriptome analysis and qPCR validation showed that BFP-TA could alleviate inflammation, oxidative stress, apoptosis and lipid metabolism disorders by regulating the expression of DEGs in PPAR and PI3K-Akt signaling pathways, thereby exerting a protective effect against CSE-induced Beas-2B cell injury.

Conclusion: This study is the first to demonstrate that BFP-TA could exert a protective effect on CSE-induced Beas-2B cell injury by exerting anti-inflammatory, antioxidant, anti-apoptotic and regulate lipid metabolism disorders.

References
1.
Xu W, Li F, Zhu L, Cheng M, Cheng Y . Pacenta polypeptide injection alleviates the fibrosis and inflammation in cigarette smoke extracts-induced BEAS-2B cells by modulating MMP-9/TIMP-1 signaling. J Biochem Mol Toxicol. 2023; 37(11):e23453. DOI: 10.1002/jbt.23453. View

2.
Fujii W, Kapellos T, Bassler K, Handler K, Holsten L, Knoll R . Alveolar macrophage transcriptomic profiling in COPD shows major lipid metabolism changes. ERJ Open Res. 2021; 7(3). PMC: 8435801. DOI: 10.1183/23120541.00915-2020. View

3.
Adam G, Shiomi T, Monica G, Jarrod S, Vincent A, Becky M . Suppression of cigarette smoke induced MMP1 expression by selective serotonin re-uptake inhibitors. FASEB J. 2021; 35(7):e21519. PMC: 9292461. DOI: 10.1096/fj.202001966RR. View

4.
Liu Y, Kong H, Cai H, Chen G, Chen H, Ruan W . Progression of the PI3K/Akt signaling pathway in chronic obstructive pulmonary disease. Front Pharmacol. 2023; 14:1238782. PMC: 10548138. DOI: 10.3389/fphar.2023.1238782. View

5.
Kahnert K, Jorres R, Behr J, Welte T . The Diagnosis and Treatment of COPD and Its Comorbidities. Dtsch Arztebl Int. 2023; 120(25):434-444. PMC: 10478768. DOI: 10.3238/arztebl.m2023.027. View