1,25-Dihydroxy Vitamin D3 Attenuates the Oxidative Stress-Mediated Inflammation Induced by PM2.5via the p38/NF-κB/NLRP3 Pathway

Xin, Lili; Che, Bizhong; Zhai, Bingzhong; Luo, Qian; Zhang, Chen; Wang, Jianshu; Wang, Shengli; Fan, Guoqiang; Liu, Zhiyong; Feng, Jialiang; Zhang, Zengli

doi:10.1007/s10753-018-0928-y

Cited by 42 publications

(30 citation statements)

References 48 publications

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“…Our previous study supported the notion that PM 2.5 exposure induces aberrant activation of NF- к B signalling in human airway epithelial cells [ 15 , 18 , 20 , 21 ]. Active NF- к B can be translocated from the cytosol to the nucleus, where it activates the transcription of various genes, including IL-6, tumour necrosis factor- α (TNF- α ), interluekin-1 β (IL-1 β ), and inducible nitric oxide synthase (iNO S ), which are involved in the inflammatory response and lead to cell injury [ 22 ].…”

Section: Discussionsupporting

confidence: 88%

Calycosin Alleviates Injury in Airway Epithelial Cells Caused by PM 2.5 Exposure via Activation of AMPK Signalling

Wang

Luo

Bai

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Introdution. Calycosin, a major active component in Astragali radix, has antitumour and anti-inflammation properties, but its effects on PM 2.5-induced injury in vitro and in vivo have not been clarified. Methods. Phospho-AMP-activated protein kinase (p-AMPK) and AMP-activated protein kinase (AMPK) were detected by western blot. Immunofluorescence staining was used to validate changes in the levels of nuclear factor kappa B (NF-кB) p65 nuclear translocation. Mice were administered intraperitoneally with calycosin one hour before anaesthesia and endotracheal instillation of PM 2.5. The extent of lung injury was evaluated in the H&E-stained lung sections. Apoptotic cells were detected by TUNEL staining. Results. Administration of calycosin was increased in PM 2.5-treated B2B cells in a dose-dependent manner in vitro. Fluorescence signals from anti-NF-кB p65 were increased in nuclei of cells pretreated with calycosin. The level of p-AMPK was increased by calycosin in vitro and in vivo. After pretreatment with compound C, the inhibitory effects of calycosin on cytotoxicity, levels of inflammatory cytokines and p-AMPK, and levels of NF-кB p65 nuclear translocation were not significantly decreased in vitro or in vivo. Conclusions. Calycosin effectively decreased the release of inflammatory cytokines and alleviated injury caused by PM 2.5. These effects were mediated through activation of AMPK to suppress NF-κB signalling.

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Section: Discussionsupporting

confidence: 88%

Calycosin Alleviates Injury in Airway Epithelial Cells Caused by PM 2.5 Exposure via Activation of AMPK Signalling

Wang

Luo

Bai

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Although the exact etiology of UC remains uncertain, activation of NF‐κB pathway is related to both pathogenesis and exacerbation of UC. Activated NF‐κB signaling pathway released pro‐inflammatory factors IL‐6, IL‐1β and TNF‐α (Liang et al, 2017; Xin et al, 2019), which in turn further activated NF‐κB pathway, and promoted the pathogenesis of UC. In resting state, NF‐κB locates in cytoplasm and binds to inhibitory protein IκBs (Shi, Lindholm, & Sarna, 2003), when being stimulated by inflammatory response mediators, IκBs are phosphorylated by IKKs, then being degraded by proteases, eventually activate NF‐κB signaling (Wang, Tang, Duan, & Yang, 2018).…”

Section: Discussionmentioning

confidence: 99%

Apple polyphenols extract alleviated dextran sulfate sodium‐induced ulcerative colitis in C57BL/6 male mice by restoring bile acid metabolism disorder and gut microbiota dysbiosis

Liu

Wang

Liu

et al. 2020

Phytotherapy Research

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To investigate and compare the preventive effects of apple polyphenols extract (APE) with phloretin on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC), 60 male mice were treated with 125 or 500 mg/(kg bw d) APE or 100 mg/(kg bw d) phloretin, the single-ingredient of APE, for continuous 3 weeks by intragastric administration, meanwhile, mice were provided with 3% DSS dissolved in drinking water to induce UC during the third week. Both APE and phloretin significantly ameliorated DSS-induced UC by inhibiting body weight loss, preventing colon shortening and mucosa damage. Except the same mechanisms of the inhibited activation of NF-κB signaling, decreased hyodeoxycholic acid level and increased abundance of Verrucomicrobia at phylum and Bacteroides and Akkermansia at genus, APE increased β-muricholic acid level and decreased Bacterodetes abundance, while phloretin decreased Firmicutes abundance. Furthermore, APE treatment showed much lower disease activity index score, less body weight loss and lighter spleen than phloretin. Thus, our study supported the potentiality of APE as a promising dietary intervention for the prevention of experimental UC.

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“…Low levels of VitD3 observed in the serum of infants and women have been associated with high levels of air pollution [ 194 , 195 ], making it a potential target for therapy. Of note, 1 day pre-treatment with VitD3 diminished PM 2.5 -induced increase in ROS and activation of NF-κB in AECs [ 196 ], which may lead to reduction in ROS-mediated barrier damage. Furthermore, VitD3 supplementation suppressed TGFβ-induced decrease in E-cadherin in AECs and inhibited epithelial-mesenchymal transition (EMT) [ 197 ].…”

Section: Therapeutic Strategies For Restoration Of Airway Epithelial ...mentioning

confidence: 99%

Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD

et al. 2022

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Chronic exposure to environmental pollutants is a major contributor to the development and progression of obstructive airway diseases, including asthma and COPD. Understanding the mechanisms underlying the development of obstructive lung diseases upon exposure to inhaled pollutants will lead to novel insights into the pathogenesis, prevention and treatment of these diseases. The respiratory epithelial lining forms a robust physicochemical barrier protecting the body from inhaled toxic particles and pathogens. Inhalation of airborne particles and gases may impair airway epithelial barrier function and subsequently lead to exaggerated inflammatory responses and airway remodelling, which are key features of asthma and COPD. In addition, air pollutant-induced airway epithelial barrier dysfunction may increase susceptibility to respiratory infections, thereby increasing the risk of exacerbations and thus triggering further inflammation. In this review, we discuss the molecular and immunological mechanisms involved in physical barrier disruption induced by major airborne pollutants and outline their implications in the pathogenesis of asthma and COPD. We further discuss the link between these pollutants and changes in the lung microbiome as a potential factor for aggravating airway diseases. Understanding these mechanisms may lead to identification of novel targets for therapeutic intervention to restore airway epithelial integrity in asthma and COPD.

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1,25-Dihydroxy Vitamin D3 Attenuates the Oxidative Stress-Mediated Inflammation Induced by PM2.5via the p38/NF-κB/NLRP3 Pathway

Cited by 42 publications

References 48 publications

Calycosin Alleviates Injury in Airway Epithelial Cells Caused by PM 2.5 Exposure via Activation of AMPK Signalling

Calycosin Alleviates Injury in Airway Epithelial Cells Caused by PM 2.5 Exposure via Activation of AMPK Signalling

Apple polyphenols extract alleviated dextran sulfate sodium‐induced ulcerative colitis in C57BL/6 male mice by restoring bile acid metabolism disorder and gut microbiota dysbiosis

Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD

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