Resveratrol prevents nanoparticles-induced inflammation and oxidative stress via downregulation of PKC-α and NADPH oxidase in lung epithelial A549 cells

Hsu, Hung-Te; Tseng, Yu‐Ting; Wong, Wen-Jhe; Liu, Chi-Ming; Lo, Yi-Ching

doi:10.1186/s12906-018-2278-6

Cited by 43 publications

(25 citation statements)

References 51 publications

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“…Chemical inhibition of AhR and NF-jB by Res significantly attenuated the Pb-induced oxidative stress by reducing the formation of ROS and restored the expression of GSTA1, iNOS, and CYP1A1 in A549 cells exposed to Pb. In agreement with our results, it has been reported that Res prevents nanoparticles-induced inflammation and oxidative stress in A549 cells via inhibition of ROS production and oxidative stress (Hsu et al 2018). In addition, since activation of AhR/ CYP1A1 pathway by Pb is always associated with increased oxidative stress, we postulate here that blocking of AhR would explain the inhibitory effect of Res on ROS production.…”

Section: Control (B)supporting

confidence: 93%

The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

Attafi

Bakheet

Korashy

2019

Toxicology Mechanisms and Methods

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Lead (Pb) is recognized as the first heavy metal of the top six toxic air pollutants threatening human health and the second hazardous substance. Pb exposure is associated with lung impairment and high incidences of lung cancer. Nuclear factor kappa B (NF-jB) and aryl hydrocarbon receptor (AhR) signaling pathways are known to be expressed and play an important role in the lung. However, the link between Pb lung toxicity and NF-jB and/or AhR pathways remains unclear. This study was established to explore the role of NF-jB and AhR modulation in Pb-induced lung toxicity in human lung cancer A549 cells. In the current study, treatment of A549 cells with Pb significantly induced cell apoptosis as evidenced by increasing a) the percentage of cells underwent apoptosis determined by flow cytometry and b) p53 mRNA level. Pb treatment induced oxidative stress by a) increasing the formation of reactive oxygen species and b) decreasing GSTA1 mRNA levels. The toxic effects of Pb on the lung was associated with significant increases in NF-jB and AhR levels which was accompanied with increases in downstream targets genes, iNOS and CYP1A1, respectively. Inhibition of NF-jB or AhR either chemically using resveratrol or genetically using small interfering RNA (siRNA) significantly rescued A549 cells from Pb-mediated lung toxicity. The results clearly indicate that Pb-mediated lung toxicities are NF-jB and AhR-dependent mechanism.

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Section: Control (B)supporting

confidence: 93%

The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

Attafi

Bakheet

Korashy

2019

Toxicology Mechanisms and Methods

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“…Oxidative Medicine and Cellular Longevity resveratrol could also alleviate oxidative and inflammatory factors via inhibiting PKC-α/NOX2 signaling pathway [33]. In our present study, we also confirmed the relationship between PKC-α and NOX2 in U937 monocytes.…”

supporting

confidence: 86%

“…PKC activation also has been identified to play an important part in inflammation and oxidative stress [31,32]. It has been reported that the cross talk between PKC and NOX could induce NOX-dependent ROS production [33]. In rat brain astrocytes, bradykinin could induce inflammation via activating PKC-α-mediated NOX2/ROS signaling pathway [34].…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

Chai

Cao

et al. 2020

Oxidative Medicine and Cellular Longevity

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Dexmedetomidine is widely used for sedating patients in operation rooms or intensive care units. Its protective functions against oxidative stress, inflammation reaction, and apoptosis have been widely reported. In present study, we explored the effects of dexmedetomidine on monocyte-endothelial adherence. We built lipopolysaccharide- (LPS-) induced monocyte-endothelial adherence models with U937 monocytes and human umbilical vein endothelial cells (HUVECs) and observed the effects of dexmedetomidine on U937-HUVEC adhesion. Specific siRNA was designed to knock-down Connexin43 (Cx43) expression in U937 monocytes. Gö6976, GSK2795039, and NAC were used to inhibit PKC-α, NOX2, and ROS, respectively. Then, we detected whether dexmedetomidine could downregulate Cx43 expression and its downstream PKC-α/NOX2/ROS signaling pathway activation and ultimately result in the decrease of U937-HUVEC adhesion. The results showed that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), could inhibit adhesion of molecule expression (VLA-4 and LFA-1) and U937-HUVEC adhesion. Simultaneously, it also attenuated Cx43 expression in U937 monocytes. With the downregulation of Cx43 expression, the activity of PKC-α and its related NOX2/ROS signaling pathway were reduced. Inhibiting PKC-α/NOX2/ROS signaling pathway with Gö6976, GSK2795039, and NAC, respectively, VLA-4, LFA-1 expression, and U937-HUVEC adhesion were all decreased. In summary, we concluded that dexmedetomidine, at its clinically relevant concentrations (0.1 nM and 1 nM), decreased Cx43 expression in U937 monocytes and PKC-α associated with carboxyl-terminal domain of Cx43 protein. With the downregulation of PKC-α, the NOX2/ROS signaling pathway was inhibited, resulting in the decrease of VLA-4 and LFA-1 expression. Ultimately, U937-HUVEC adhesion was reduced.

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“…The anti-apoptotic and antioxidant stress-protective effects of RES have been widely investigated. In 2018, Hsu et al (36) revealed that RES could protect A549 human lung epithelial cells against carbon black nanoparticle (CBNP)-induced inflammation and oxidative stress, as cBNPs are known to promote pulmonary toxicity through inflammation and oxidative stress. A previous study used cigarette smoke extract (cSE), which induced apoptosis in a human bronchial epithelial cell model and studied the effects of treatment with or without RES (37).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol decreases cell apoptosis through inhibiting DNA damage in bronchial epithelial cells

et al. 2020

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One of the major risk factors for asthma development is exposure to environmental allergens. House dust mites (HdM) can induce dNA damage, resulting in asthma. Resveratrol (RES) produced by several plants, has anti-apoptotic properties and may affect a variety of biological processes. The aim of the present study was to investigate the protective role of RES against apoptosis in bronchial epithelial cells. c57BL/6J mice treated with HdM exhibited high levels of cell apoptosis, while RES significantly reversed this process. Induced dNA damage was more severe in the HdM group vs. the HdM combined with RES group. This result was confirmed by immunostaining and western blot analysis of the protein expression of the dNA damage-related gene γH2AX, which was highly induced by HdM. In addition, treatment with RES protected bronchial epithelial cells exposed to HdM from dNA damage. RES decreases reactive oxygen species levels to inhibit oxidative dNA damage in bronchial epithelial cells. Furthermore, compared with the HdM group, induced cell apoptosis could be attenuated by RES in the group of combined treatment with RES and HdM. A dNA repair inhibitor augmented dNA damage and apoptosis in bronchial epithelial cells, whereas RES significantly attenuated cell apoptosis through inhibiting dNA damage.

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Resveratrol prevents nanoparticles-induced inflammation and oxidative stress via downregulation of PKC-α and NADPH oxidase in lung epithelial A549 cells

Cited by 43 publications

References 51 publications

The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-α/NOX2/ROS Signaling Pathway in Monocytes

Resveratrol decreases cell apoptosis through inhibiting DNA damage in bronchial epithelial cells

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