Angiotensin-(1–7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats

Lu, Wenyue; Kang, Jian; Hu, Ke; Tang, Si; Zhou, Xin; Yu, Shuiliang; Li, Y.; Xu, Liang

doi:10.1590/1414-431x20165431

Cited by 31 publications

(24 citation statements)

References 35 publications

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“…For instance, hydrogen therapy was found possessing the potential of reducing irradiation-induced pulmonary oxidative stress ( Terasaki et al, 2011 ). Angiotensin-(1–7) and nitric oxide synthase inhibitor L-NAME showed inhibitive effects on pulmonary oxidative damage in rodents ( De Bittencourt Pasquali et al, 2012 ; Lu et al, 2016 ). However, there remains an urgent need for nontoxic and antioxidant therapies to prevent and remedy pulmonary oxidative damage and pulmonary fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

Lü

Liu

Zhai

et al. 2017

PeerJ

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Oxidative damage is a major cause of lung diseases, including pulmonary fibrosis. Laminarin is a kind of polysaccharide extracted from brown algae and plays vital roles in various biological processes. However, the functions and mechanisms of laminarin in pulmonary oxidative damage are poorly understood. This study aimed at investigating the protective effect of laminarin against pulmonary oxidative damage and underlying mechanisms. Human lung fibroblasts MRC-5 cells were treated with hydrogen peroxide to induce oxidative damage. Laminarin treatment was performed before or after hydrogen peroxide treatment, and then major indexes of oxidative damage, including superoxide dismutase (SOD), malondialdehyde (MDA), reduced glutathione (GSH) and catalase (CAT), were quantified by biochemical assays. The expression of oxidation-related factor, nuclear factor erythroid 2 like 2 (NRF2) was analyzed by qPCR, Western blot and immunofluorescence assay. NRF2 knockdown and overexpression were performed by cell transfection to reveal possible mechanisms. Results showed that laminarin treatment of 0.020 mg/mL for 24 h, especially the pre-treatment, could significantly relieve changes in SOD, MDA, GSH and CAT that were altered by hydrogen peroxide, and promote NRF2 mRNA (P < 0.001). NRF2 protein was also elevated by laminarin, and nuclear translocation was observed. Factors in NRF2 signaling pathways, including KEAP1, NQO1, GCLC and HO1, were all regulated by laminarin. Roles of NRF2 were tested, suggesting that NRF2 regulated the concentration of SOD, MDA, GSH and CAT, suppressed KEAP1, and promoted NQO1, GCLC and HO1. These findings suggested the protective role of laminarin against pulmonary oxidative damage, which might involve the regulation of NRF2 signaling pathways. This study provided information for the clinical application of laminarin to pulmonary diseases like pulmonary fibrosis.

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Section: Introductionmentioning

confidence: 99%

Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

Lü

Liu

Zhai

et al. 2017

PeerJ

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“…The lung tissue specimens of the rats were first fixed with 10% formalin, paraffin-embedded, cut into 5-mm-thick slices, and then stained with hematoxylin and eosin (H&E) [ 8 ]. Images were obtained using light microscopy (Nikon Instrument Group, USA).…”

Section: Methodsmentioning

confidence: 99%

“…SOD and CAT activity in lung tissues were determined by using commercial assay kits (CST) following the manufacturer’s instructions. The enzyme activity is presented as units/mg of protein [ 8 ].…”

Section: Methodsmentioning

confidence: 99%

Sinomenine Attenuates Chronic Intermittent Hypoxia-Induced Lung Injury by Inhibiting Inflammation and Oxidative Stress

et al. 2018

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BackgroundIn the present study, we aimed to investigate the effects of sinomenine (SIN) on chronic intermittent hypoxia (CIH)- induced lung injury in rats, and to explore the underlying mechanisms.Material/MethodsTo perform the investigation, a CIH rat model was established. ELISA assay was applied to detect the level of inflammatory cytokines. Oxidative stress bio-markers (MDA, SOD, and CAT) were determined in lung tissues. In addition, the expression level of NADPH oxidase 2 (Nox2) was analyzed by Western blotting and qRT-PCR, respectively.ResultsThe results showed that compared with other groups, more obvious pulmonary pathological changes were observed in the CIH group. The level of inflammatory cytokines in the CIH group was markedly higher than that in the control and Con-S groups. Compared with the control and Con-S groups, oxidative stress was notably increased in the CIH group. Expression of Nox2 was also increased in the CIH group. The effects caused by CIH in rats were attenuated by SIN treatment.ConclusionsSIN can reverse chronic intermittent hypoxia-induced lung injury through inhibiting inflammation and oxidative stress.

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“…Commercial colorimetric detection kits were used to assay the level of MDA and enzymatic activities of SOD and CAT in children with or without ankle fracture and MG-63 cells in accordance with the manufacturer’s instructions. The enzyme activity in cells is presented as units/mg of protein [ 20 ].…”

Section: Methodsmentioning

confidence: 99%

Sinomenine Regulates Inflammatory Response and Oxidative Stress via Nuclear Factor kappa B (NF-κB) and NF-E2-Related Factor 2 (Nrf2) Signaling Pathways in Ankle Fractures in Children

et al. 2018

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BackgrounThis study aimed to investigate the effects of SIN on ankle fracture and the underlying mechanisms in MG-63 cells.Mateeial/MethodsqRT-PCR and ELISA assay were used to detect the mRNA and protein levels of cytokines in peripheral blood of children with or without ankle fracture. The expression and activity of antioxidant and detoxifying enzymes were detected by ELISA assay. Pretreated MG-63 cells with/without SIN were stimulated with 1 μg/ml bradykinin (BK). A CCK-8 kit was used to detect the cell viability. The cytokines produced from MG-63 cells were detected by Western blotting and qRT-PCR. Moreover, Western blotting was used to detect the levels of p-p38 and p-NF-κB (p65), and the activation level of the Nrf2 signaling pathway was examined by qRT-PCR and Western blotting.ResultsIn this study, we found that compared with the healthy children, the mRNA and protein levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were significantly upregulated in children with ankle fracture. In addition, the expression and activity of antioxidant and detoxifying enzymes were imbalanced in children with ankle fracture. SIN treatment did not have a cytotoxic effect on MG-63 cells. SIN dose-dependently suppressed BK-induced upregulation of IL-1β, IL-6, TNF-α, p-p38, and p-NF-κB (p65). Furthermore, SIN dramatically inhibited oxidative stress induced by BK via balancing the expression and activity of antioxidant and detoxifying enzymes and inhibited the activation of Nrf2 signaling.ConclusionsSIN might be a potential agent for the treatment of ankle fracture through reducing inflammatory response and oxidative stress.

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Angiotensin-(1–7) inhibits inflammation and oxidative stress to relieve lung injury induced by chronic intermittent hypoxia in rats

Cited by 31 publications

References 35 publications

Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

Laminarin protects against hydrogen peroxide-induced oxidative damage in MRC-5 cells possibly via regulating NRF2

Sinomenine Attenuates Chronic Intermittent Hypoxia-Induced Lung Injury by Inhibiting Inflammation and Oxidative Stress

Sinomenine Regulates Inflammatory Response and Oxidative Stress via Nuclear Factor kappa B (NF-κB) and NF-E2-Related Factor 2 (Nrf2) Signaling Pathways in Ankle Fractures in Children

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