Nebulized lidocaine ameliorates allergic airway inflammation via downregulation of TLR2

Wang, Lixia; Wang, Muzi; Li, Shuai; Wu, Hui-Mei; Shen, Qiying; Zhang, Shihai; Fang, Lei; Liu, Rong‐Yu

doi:10.1016/j.molimm.2018.03.010

Cited by 32 publications

(22 citation statements)

References 39 publications

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“…It is widely used in regional anaesthesia, peripheral nerve blocks, and epidural anaesthesia with excellent effects on the management of pain. Beyond that, lidocaine also has many other pharmacological effects, like antipyroptosis [5], neuroprotection [6], cerebral protection [7], anti-inflammation [8], preventing mitochondrial dysfunction [9], and so forth. Moreover, recently paper reported the antitumour properties of lidocaine against diverse cancers, including colon adenocarcinoma [10], gastric cancer [11], breast cancer [12], and lung cancer [13].…”

Section: Introductionmentioning

confidence: 99%

Lidocaine inhibits proliferation and metastasis of lung cancer cell via regulation of miR-539/EGFR axis

Sun

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Despite the medical uses of lidocaine has been well-characterized, the study of lidocaine's pharmacological function other the anaesthetic effect was never stopped. This study designed to reveal the effect of lidocaine on the growth and metastasis of lung cancer in vitro. Methods: A549 and NCI-H1299 cells were treated by lidocaine for 24 h. miR-539 expression in cell was silenced by transfection with the specific inhibitor. The changes in cell growth and metastasis were determined using CCK-8 assay and western blot. Luciferase activity assay was performed to assay if EGFR was a target of miR-539. Western blot was used to test the activation of EGFR downstream signalling. Results: Lidocaine suppressed the viability, migration, and invasion of A549 and NCI-H1299 cells while induced apoptotic death. Lidocaine elevated the expression of miR-539. The anti-tumour properties of lidocaine towards A549 and NCI-H1299 cells were partially attenuated when miR-539 was silenced. EGFR was a target of miR-539. Lidocaine repressed the activation of ERK and PI3K/AKT pathways also via regulating miR-539. Conclusion: The anti-growth and anti-metastatic effects of lidocaine towards lung cancer cells. The anti-tumour properties of lidocaine may be partial via up-regulation of miR-539, which blocked EGFR signalling by directly binding with EGFR.

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Section: Introductionmentioning

confidence: 99%

Lidocaine inhibits proliferation and metastasis of lung cancer cell via regulation of miR-539/EGFR axis

Sun

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Likewise, multiple studies have shown that expression and activation of TLR2 may contribute to melanoma metastasis (31,32). The direct effects of TLR2 stimulation on the lung tissue and subsequent inflammation have been explored, however few studies to date have evaluated the effects of TLR2 stimulation among different NSCLC subtypes (33).…”

Section: Discussionmentioning

confidence: 99%

Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

et al. 2020

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Background/Aim: The aim of this study was to evaluate the role of toll-like receptor 2 (TLR2) in the proliferation of human lung cancer cells and identify the signaling pathway that mediates this effect. Materials and Methods: Adenocarcinoma (A549 and H1650) and adenosquamous (H125) cells were treated with increasing doses of Pam3CSK4, a TLR2 agonist. Cell proliferation and NF-ĸB activation were evaluated. NF-ĸB was inhibited prior to treatment with Pam3CSK4 and proliferation was assessed. Results: TLR2 expression was significantly higher in A549 and H1650 cells compared to H125 cells (p<0.001). TLR2 stimulation induced proliferation in adenocarcinoma cells only and led to a corresponding increase in NF-ĸB activity (p<0.05). Inhibition of NF-ĸB prior to treatment with Pam3CSK4 attenuated this proliferative response. Conclusion: TLR2 activation induced proliferation of lung adenocarcinoma cells through activation of NF-ĸB. Thus, the TLR2 signaling pathway may be a potential therapeutic target in lung adenocarcinoma.

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“…injection of 10 μg OVA (Sigma, St. Louis, MO, U.S.A.) complexed with 1 mg potassium aluminum sulphate (Sangon Biotech, Shanghai, China) in 0.5 Ml of saline. Subsequently, mice were exposed to aerosolized 1% OVA for 30 min per day from day 14 to 20 using an ultrasonic nebulizer device [28]. Sham and OVX groups were saline-sensitized and challenged instead of OVA-aluminum solution.…”

Section: Methodsmentioning

confidence: 99%

Estrogen ameliorates allergic airway inflammation by regulating activation of NLRP3 in mice

Cheng

Wang

et al. 2019

Bioscience Reports

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Background: Estrogen has been suggested to play a protective role against airway inflammations, such as asthma. In these processes, the inflammasome nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3 (NLRP3) partly accounts for the activation of pro-inflammatory factors. The aim of the present study was to investigate whether NLRP3 was involved in the protective effect of estrogen against allergic airway inflammation. Methods: An ovariectomy was performed on female C57BL/6 mice; some were sham-operated (sham). We then sensitized and challenged them with ovalbumin (OVA) to establish an airway inflammation model. Meanwhile, some mice were treated with 17β-estradiol (E2) for 28 days. Results: The expression of NLRP3 inflammasome and its downstream products, caspase-1 and the pro-inflammatory cytokine interleukin (IL)-1β (IL-1β), increased concomitantly with OVA-challenged airway inflammation and decreased with the expression of estrogen receptor β (ERβ). In addition, treating ovariectomized (OVX) mice with E2 dramatically ameliorated airway inflammation via such mechanisms as leukocyte recruitment, mucus production, and secretion of pro-inflammatory cytokines other than IL-18 in bronchoalveolar lavage (BAL) fluid (BALF). Furthermore, E2 suppressed both the mRNA expression and protein expression of NLRP3, caspase-1, and IL-1β. In summary, our study showed that NLRP3 inflammasome activation and pro-inflammatory cytokine production markedly increased in OVA-induced airway inflammation, and E2 effectively abrogated such inflammation by regulating the activation of NLRP3.

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Nebulized lidocaine ameliorates allergic airway inflammation via downregulation of TLR2

Cited by 32 publications

References 39 publications

Lidocaine inhibits proliferation and metastasis of lung cancer cell via regulation of miR-539/EGFR axis

Lidocaine inhibits proliferation and metastasis of lung cancer cell via regulation of miR-539/EGFR axis

Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

Estrogen ameliorates allergic airway inflammation by regulating activation of NLRP3 in mice

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