Pinellia ternata (Thunb.) Breit. attenuates the allergic airway inflammation of cold asthma via inhibiting the activation of TLR4-medicated NF-kB and NLRP3 signaling pathway

Tao, Xing-Bao; Li, Juan; He, Jing; Jiang, Yunbin; Liu, Chun‐Shan; Cao, Weiguo; Wu, Hao

doi:10.1016/j.jep.2023.116720

Cited by 3 publications

(3 citation statements)

References 53 publications

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“…Notably, a recent study also showed that valsartan mitigated sepsis-induced lung damage via modulating macrophage ( Zhang et al, 2016 ; Jangam et al, 2023 ). Additionally, previous studies have demonstrated that activation of the MAPK signaling pathway (including ERK, JNK, and p38 cascades) and NF-κB signaling pathway promote MUC5AC expression as well as inflammatory cytokines/chemokines expression in human airway epithelial cells ( Ha et al, 2008 ; Nie et al, 2012 ; Tao et al, 2023 ; Zhou et al, 2023 ). Therefore, valsartan may inhibit the expression of MUC5AC and cytokines/chemokines by downregulating the MAPK and NF-κB signaling pathways in LPS-induced ALI model in this study.…”

Section: Discussionmentioning

confidence: 97%

“…Previous studies have indicated that it has anti-inflammatory and anti-oxidative effects. Valsartan prevents gefitinib-induced lung inflammation and oxidative stress, modulates plasma metabolites in rats, and attenuates gefitinib-induced cardiac hypertrophy in rat by modulating angiotensin II-mediated oxidative stress and the JNK/P38 pathway ( Nie et al, 2012 ; Tao et al, 2023 ). Additionally, telmisartan, another angiotensin II type 1 receptor antagonist, has been found to attenuate LPS-induced MUC5AC production by upregulating cytokine signaling inhibitory factor 1 (SOCS1) ( Chen et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

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Valsartan attenuates LPS-induced ALI by modulating NF-κB and MAPK pathways

Zhou,

Meng,

et al. 2024

Front. Pharmacol.

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Background: Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a common respiratory disease characterized by persistent hypoxemia and an uncontrolled inflammatory response. Valsartan, an angiotensin II type 1 receptor antagonist, is clinically used to treat hypertension and has anti-inflammatory and antioxidant effects on gefitinib-induced pneumonia in rats. However, the potential therapeutic effects of valsartan on lipopolysaccharide (LPS)-induced ALI remain unclear. This study investigated the protective role of valsartan in LPS-induced ALI and its underlying mechanisms.Methods: LPS-treated BEAS-2B cells and ALI mouse model were established. BEAS-2B cells were treated with LPS (10 μg/mL) for 24h, with or without valsartan (20, 40, and 80 µM). For ALI mouse models, LPS (5 mg/kg) was administered through intratracheal injection to treat the mice for 24h, and valsartan (10 or 30 mg/kg) was injected intraperitoneally twice 2 h before and 12 h after the LPS injection. Pulmonary functional parameters were examined by an EMKA pulmonary system. Hematoxylin and eosin staining, flow cytometry, CCK-8 assay, qRT-PCR, ELISA, immunofluorescence, Western blotting, and related commercial kits were used to assess the pathological damage to the lungs, neutrophil recruitment in the lung tissue and bronchoalveolar lavage fluid (BALF), cell viability, inflammation, oxidative activity, and mucus production, respectively. Potential mechanisms were further explored using network pharmacology and Western blotting.Results: Valsartan rescued LPS-reduced cell viability of BEAS-2B cells, improved the pulmonary function, ameliorated pathological lung injury in mice with ALI, ameliorated LPS-induced neutrophil recruitment in BALF and lung tissue of mice, attenuated oxidative stress by increasing the level of SOD and decreasing that of MDA and GSSG, inhibited LPS-induced MUC5AC overproduction, decreased the LPS-induced increase in expression of pro-inflammatory cytokines/chemokines including TNF-α, IL-6, IL-1β, CXCL-1 and CXCL-2, and restored the expression of anti-inflammatory IL-10. Mechanistic studies showed that valsartan inhibits LPS-induced phosphorylation of nuclear factor-kappa B (NF-κΒ) and mitogen-activated protein kinases (MAPKs) including P38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) in both LPS-treated cells and the mouse model of ALI.Conclusion: Valsartan protects against LPS-induced ALI by attenuating oxidative stress, reducing MUC5AC production, and attenuating the inflammatory response that may involve MAPK and NF-κΒ pathways.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Valsartan attenuates LPS-induced ALI by modulating NF-κB and MAPK pathways

Zhou,

Meng,

et al. 2024

Front. Pharmacol.

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“…TLRs can activate multiple intracellular signals, including the nuclear factor κB (NF-κB) pathway, which plays a major role in regulating inflammatory responses [25]. Recent research has indicated that NF-κB serves as an integral component of the initiation signal required for stimulation of the NLRP3 inflammasome, which subsequently triggers the activation of Caspase-1 and consequent release of interleukin (IL)-1β [26,27]. TLR-mediated inflammation is implicated in pulmonary diseases including asthma, pulmonary fibrosis, and chronic obstructive pulmonary disease (COPD) [28][29][30][31][32].…”

Section: Introductionmentioning

confidence: 99%

Pulmonary toxicity assessment of polypropylene, polystyrene, and polyethylene microplastic fragments in mice

Kwabena Danso,

Woo,

Hoon Baek

et al. 2024

Toxicol Res.

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Polypropylene (PP), polystyrene (PS), and polyethylene (PE) plastics are commonly used in household items such as electronic housings, food packaging, bottles, bags, toys, and roofing membranes. The presence of inhalable microplastics in indoor air has become a topic of concern as many people spent extended periods of time indoors during the COVID-19 pandemic lockdown restrictions, however, the toxic effects on the respiratory system are not properly understood. We examined the toxicity of PP, PS, and PE microplastic fragments in the pulmonary system of C57BL/6 mice. For 14 days, mice were intratracheally instilled 5 mg/kg PP, PS, and PE daily. The number of inflammatory cells such as macrophages, neutrophils, and eosinophils in the bronchoalveolar lavage fluid (BALF) of PS-instilled mice was significantly higher than that in the vehicle control (VC). The levels of inflammatory cytokines and chemokines in BALF of PS-instilled mice increased compared to the VC. However, the inflammatory responses in PP- and PE-stimulated mice were not significantly different from those in the VC group. We observed elevated protein levels of toll-like receptor (TLR) 2 in the lung tissue of PP-instilled mice and TLR4 in the lung tissue of PS-instilled mice compared with those to the VC, while TLR1, TLR5, and TLR6 protein levels remained unchanged. Phosphorylation of nuclear factor kappa B (NF-κB) and IĸB-α increased significantly in PS-instilled mice compared with that in VC. Furthermore, Nucleotide‑binding oligomerization domain‑like receptor family pyrin domain‑containing 3 (NLRP3) inflammasome components including NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and Caspase-1 in the lung tissue of PS-instilled mice increased compared with that in the VC, but not in PP- and PE-instilled mice. These results suggest that PS microplastic fragment stimulation induces pulmonary inflammation due to NF-ĸB and NLRP3 inflammasome activation by the TLR4 pathway.

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