Inhibition of LPS-induced Nox2 activation by VAS2870 protects alveolar epithelial cells through eliminating ROS and restoring tight junctions

Li, Dan; Cong, Zhukai; Yang, Cui; Zhu, Xi

doi:10.1016/j.bbrc.2020.01.134

Cited by 18 publications

(15 citation statements)

References 29 publications

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“…Next, we wanted to determine whether exposure to PM altered levels and/or localization of tight junction proteins, since redox status has been previously shown to regulate levels and localization of these proteins [25][26][27]. First, we analysed the effects of PM exposure on the levels of zonula occludens protein 1 (ZO−1).…”

Section: Pm Exposure Of 3d Human Intestinal Tissues Decreases Levels Of Tight Junction Proteins and Desmocollinmentioning

confidence: 99%

“…These junctions are located on the lateral side of plasma membranes and are composed of cadherin family members, including desmocollin, that can interact with each other via their extracellular domains and are associated with the cytoskeleton through interactions with specific desmosomal plaque proteins [21][22][23][24]. Interestingly, redox status has been shown to regulate the levels and localization of proteins involved in intestinal barrier function [25][26][27].…”

Section: Introductionmentioning

confidence: 99%

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Particulate Matter Decreases Intestinal Barrier-Associated Proteins Levels in 3D Human Intestinal Model

Woodby

Schiavone

Pambianchi

et al. 2020

IJERPH

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(1) Background: The gastrointestinal tract (GI) tract is one of the main organs exposed to particulate matter (PM) directly through ingestion of contaminated food or indirectly through inhalation. Previous studies have investigated the effects of chronic PM exposure on intestinal epithelia in vitro using Caco−2 cells and in vivo using mice. In this study, we hypothesized that chronic PM exposure would increase epithelial permeability and decrease barrier function due to altered redox homeostasis, which alters levels and/or localization of barrier-associated proteins in human three-dimensional (3D) intestinal tissues. (2) Methods: Transepithelial electrical resistance (TEER) in tissues exposed to 50, 100, 150, 250, and 500 µg/cm2 of PM for 1 week and 2 weeks was analyzed. Levels and localization of tight junction proteins zonula occludens protein 1 (ZO−1) and claudin−1 and desmosome-associated desmocollin were analyzed using immunofluorescence. As a marker of oxidative stress, levels of 4-hydroxy-nonenal (4HNE) adducts were measured. (3) Results: No differences in TEER measurements were observed between exposed and un-exposed tissues. However, increased levels of 4HNE adducts in exposed tissues were observed. Additionally, decreased levels of ZO−1, claudin−1, and desmocollin were demonstrated. (4) Conclusion: These data suggest that chronic PM exposure results in an increase of oxidative stress; modified levels of barrier-associated proteins could possibly link to GI tract inflammatory conditions.

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Section: Pm Exposure Of 3d Human Intestinal Tissues Decreases Levels Of Tight Junction Proteins and Desmocollinmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Particulate Matter Decreases Intestinal Barrier-Associated Proteins Levels in 3D Human Intestinal Model

Woodby

Schiavone

Pambianchi

et al. 2020

IJERPH

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“…They are activated by LPS and the release of inflammatory mediators (such as IL-6, IL-8, TNF-α, intercellular adhesion molecule 1 [ICAM-1], and PGE2), resulting in structural damage, dysfunction, apoptosis, and necrosis of cells. 36 – 40 A549 cells are widely used in studies on the injury protection mechanism of AECs. 41 Therefore, in this study, we also found that the treatment of A549 cells with endotoxins could cause A549 cells to secrete inflammatory mediators such as IL-6, IL-8, TNF-α, and PGE2.…”

Section: Discussionmentioning

confidence: 99%

Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression

et al. 2021

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In China, baicalin is the main active component of Scutellaria baicalensis, which has been used in the treatment of inflammation-related diseases, such as inflammation-induced acute lung injury. However, its specific mechanism remains unclear. This study examined the protective effect of baicalin on LPS-induced inflammation injury of alveolar epithelial cell line A549 and explored its protective mechanism. Compared with the LPS-induced group, the proliferation inhibition rates of alveolar type II epithelial cell line A549 intervened by different concentrations of baicalin decreased significantly, as did the levels of inflammatory factors IL-6, IL-1β, prostaglandin 2 and TNF-α in the supernatant. The expression levels of inflammatory proteins inducible NO synthase (iNOS), NF-κB65, phosphorylated ERK (p-ERK1/2), and phosphorylated c-Jun N-terminal kinase (p-JNK1) significantly decreased, as did the protein expression of follistatin-like protein 1 (FSTL1). In contrast, expression of miR-200b-3p significantly increased in a dose-dependent manner. These results suggested that baicalin could significantly inhibit the expression of inflammation-related proteins and improve LPS-induced inflammatory injury in alveolar type II epithelial cells. The mechanism may be related to the inhibition of ERK/JNK inflammatory pathway activation by increasing the expression of miR-200b-3p. Thus, FSTL1 is the regulatory target of miR-200b-3p.

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“…Excessive ROS production can trigger endoplasmic reticulum (ER) stress (ERS), which is called ROS-mediated ERS (17). ERS is one of the mechanisms contributing to ROS-mediated cell apoptosis (18), and ERS-associated cardiomyocyte apoptosis has been reported to be a major contributor to myocardial injury (19). The ER is responsible for the folding of secretory and membrane proteins.…”

Section: Introductionmentioning

confidence: 99%

Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress

et al. 2021

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Sepsis-induced myocardial dysfunction is one of the features of multiple organ dysfunction in sepsis, which is associated with extremely high mortality and is characterized by impaired myocardial compliance. To date, there are few effective treatment options available to cure sepsis. Tannic acid (TA) is reportedly protective during sepsis; however, the underlying mechanisms by which TA protects against septic heart injury remain elusive. The present study investigated the potential effects and underlying mechanisms of TA in alleviating lipopolysaccharide (LPS)-induced H9C2 cardiomyocyte cell apoptosis. H9C2 cells were treated with LPS (15 µg/ml), TA (10 µM) and TA + LPS; control cells were treated with medium only. Apoptosis was measured using flow cytometry, reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis. Additionally, the levels of cellular reactive oxygen species (ROS), malondialdehyde and nicotinamide adenine dinucleotide phosphate were evaluated. Western blotting and RT-qPCR were also employed to detect the expression levels of endoplasmic reticulum (ER) stress-associated functional proteins. The present findings demonstrated that TA reduced the degree of LPS-induced H9C2 cell injury, including inhibition of ROS production and ER stress (ERS)-associated apoptosis. ERS-associated functional proteins, including activating transcription factor 6, protein kinase-like ER kinase, inositol-requiring enzyme 1, spliced X box-binding protein 1 and C/EBP-homologous protein were suppressed in response to TA treatment. Furthermore, the expression levels of ERS-associated apoptotic proteins, including c-Jun N-terminal kinase, Bax, cytochrome c, caspase-3, caspase-12 and caspase-9 were reduced following treatment with TA. Additionally, the protective effects of TA on LPS-induced H9C2 cells were partially inhibited following treatment with the ROS inhibitor N-acetylcysteine, which demonstrated that ROS mediated ERS-associated apoptosis and TA was able to decrease ROS-mediated ERS-associated apoptosis. Collectively, the present findings demonstrated that the protective effects of TA against LPS-induced H9C2 cell apoptosis may be associated with the amelioration of ROS-mediated ERS. These findings may assist the development of potential novel therapeutic methods to inhibit the progression of myocardial cell injury.

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Inhibition of LPS-induced Nox2 activation by VAS2870 protects alveolar epithelial cells through eliminating ROS and restoring tight junctions

Cited by 18 publications

References 29 publications

Particulate Matter Decreases Intestinal Barrier-Associated Proteins Levels in 3D Human Intestinal Model

Particulate Matter Decreases Intestinal Barrier-Associated Proteins Levels in 3D Human Intestinal Model

Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression

Tannic acid alleviates lipopolysaccharide‑induced H9C2 cell apoptosis by suppressing reactive oxygen species‑mediated endoplasmic reticulum stress

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