Heme Oxygenase-1 Mediates Oxidative Stress and Apoptosis in Coxsackievirus B3-Induced Myocarditis

Ursu, Oana; Sauter, Martina; Ettischer, Nicole; Kandolf, Reinhard; Klingel, Karin

doi:10.1159/000356649

Cited by 37 publications

(32 citation statements)

References 33 publications

(43 reference statements)

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“…by inhibition of iNOS in macrophages of mice [43]. The activity of iNOS increased with all tested concentrations of equol used here with chicken macrophages, contrasting with equol inhibiting nitric oxide content and iNOS gene expression in murine macrophages [42].…”

Section: Discussionmentioning

confidence: 72%

Equol Inhibits LPS-Induced Oxidative Stress and Enhances the Immune Response in Chicken HD11 Macrophages

Gou

Jiang

Zheng

et al. 2015

Cell Physiol Biochem

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Background/Aims: There has been increasing recent attention on the antioxidative capacity of equol. This study tested the effect of equol on oxidative stress induced by lipopolysaccharide (LPS) and regulation of immunity in chicken macrophages. Methods: Chicken HD11 macrophages were challenged with LPS (100 ng/mL) alone or with LPS (100 ng/mL) and (±)equol (10, 20, 40, 80, 160 μmol/L) together for 24h. Evaluated responses included the contents of malondialdehyde (MDA) and reduced glutathione (GSH), activities of total superoxide dismutase (T-SOD) and inducible nitric oxide synthase (iNOS), transcript abundance of superoxide dismutase 2 (SOD2), catalase (CAT), glutathione transferase (GST), Toll-like receptor 4 (TLR4), tumor necrosis factor alpha (TNFα) and interleukin-1 beta (IL-1β), and contents of the cytokines TNFα, IL-1β, interleukin-2 (IL-2) and interferon beta (IFNβ). Results: Exposure to LPS induced oxidative stress as contents of MDA increased and GSH decreased in LPS-treated cells (P < 0.05) compared to those in control cells. Compared to LPS alone, co-treatment with equol (20 μmol/L, 40 μmol/L or 80 μmol/L) reduced contents of MDA and increased those of GSH (both P < 0.05). Activity of T-SOD increased (P < 0.05) in cells treated with the higher contentration of equol (80 μmol/L or 160 μmol/L), however, all concentrations (20 μmol/L to 160 μmol/L) increased activity of iNOS (P < 0.05). The highest concentration of equol (160 μmol/L) increased SOD2 and GST transcripts (P < 0.05). Equol treatment increased transcripts of TLR4, TNFα and IL-1β (P < 0.05). And there were similar changes in contents of IL-1β, IL-2, IFNβ and TNFα in the cells (P < 0.05). Conclusions: It concluded that equol can protect chicken HD11 macrophages from oxidative stress induced by LPS through reducing lipid peroxidation products and enhancing contents of antioxidants, and activities of relevant antioxidase enzymes; effects were also seen in gene expression related to the immune response and increased contents of cytokines. The optimal concentration of equol on antioxidation and immune enhancement in chicken macrophages was 40 μmol/L.

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Section: Discussionmentioning

confidence: 72%

Equol Inhibits LPS-Induced Oxidative Stress and Enhances the Immune Response in Chicken HD11 Macrophages

Gou

Jiang

Zheng

et al. 2015

Cell Physiol Biochem

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“…Additionally, inhibition of cell apoptosis is one of the important mechanisms that lead to the exacerbation of inflammation. Published studies show that HO-1 is capable of anti-apoptosis 47 and pro-apoptosis 1,48,49 functions depending on the cell type and disease model. In the present study, we found that up-regulation of HO-1 can promote basophil apoptosis, which contributed to the remission of allergic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Heme oxygenase‐1 inhibits basophil maturation and activation but promotes its apoptosis in T helper type 2‐mediated allergic airway inflammation

Zhong¹,

et al. 2016

Immunology

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SummaryThe anti-inflammatory role of heme oxygenase-1 (HO-1) has been studied extensively in many disease models including asthma. Many cell types are anti-inflammatory targets of HO-1, such as dendritic cells and regulatory T cells. In contrast to previous reports that HO-1 had limited effects on basophils, which participate in T helper type 2 immune responses and antigeninduced allergic airway inflammation, we demonstrated in this study, for the first time, that the up-regulation of HO-1 significantly suppressed the maturation of mouse basophils, decreased the expression of CD40, CD80, MHC-II and activation marker CD200R on basophils, blocked DQ-ovalbumin uptake and promoted basophil apoptosis both in vitro and in vivo, leading to the inhibition of T helper type 2 polarization. These effects of HO-1 were mimicked by exogenous carbon monoxide, which is one of the catalytic products of HO-1. Furthermore, adoptive transfer of HO-1-modified basophils reduced ovalbumin-induced allergic airway inflammation. The above effects of HO-1 can be reversed by the HO-1 inhibitor Sn-protoporphyrin IX. Moreover, conditional depletion of basophils accompanying hemin treatment further attenuated airway inflammation compared with the hemin group, indicating that the protective role of HO-1 may involve multiple immune cells. Collectively, our findings demonstrated that HO-1 exerted its anti-inflammatory function through suppression of basophil maturation and activation, but promotion of basophil apoptosis, providing a possible novel therapeutic target in allergic asthma.

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“…HO is the rate-limiting enzyme for degradation of heme [32]. Large amount of evidence has shown that HO plays an important in cellular protection against inflammation and oxidative stress [33][34][35][36][37]. HO-1 is an inducible isoform of HO, which plays an important role in skin injury and wound healing.…”

Section: Discussionmentioning

confidence: 99%

Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1

Li²,

Dong³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Psoriasis is one of the most common inflammatory skin disorders, affecting 3% of the general population. Terminalia chebulanin (TC) is a polyphenolic compound that possesses antioxidant and anti-inflammatory activities. The current study was designed to investigate the effect of TC on psoriatic lesions. Methods: We examined the protective effect of TC against psoriatic lesions in mice and keratinocyte proliferation in HaCaT cells. Results: We found that TC exhibited potent anti-psoriatic activities, as evidenced by improvement of erythema and scaling scores, decrease of epidermal, ear and skinfold thickening, decrease of tumor necrosis factor α (TNFα), interleukin (IL)-17A, IL-23 and matrix metalloproteinase (MMP)-9 expression, and decrease of TBARS content and increase of GSH content in IMQ-treated mice, and decrease of keratinocyte proliferation, TNFα, IL-17A and IL-23 expression, and ROS level in M5-treated cells. All those effects induced by TC were inhibited by zinc protoporphyrin IX (ZnPP), an inhibitor of heme oxygenase (HO)-1, indicating that HO-1 was responsible the anti-psoriatic effect of TC. Moreover, TC inhibited the upregulation of p65 NF-κB under in vitro psoriatic condition. ZnPP suppressed TC-induced inhibition of p65 NF-κB expression. Overexpression of p65 NF-κB significantly suppressed TC-induced decrease of TNFα, IL-17A and IL-23 expression and keratinocyte proliferation, indicating that HO-1-mediated downregulation of NF-κB was involved in the anti-psoriatic effect of TC. Conclusions: The data demonstrate that TC may serve as a potential therapeutic option for psoriatic patients.

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Heme Oxygenase-1 Mediates Oxidative Stress and Apoptosis in Coxsackievirus B3-Induced Myocarditis

Cited by 37 publications

References 33 publications

Equol Inhibits LPS-Induced Oxidative Stress and Enhances the Immune Response in Chicken HD11 Macrophages

Equol Inhibits LPS-Induced Oxidative Stress and Enhances the Immune Response in Chicken HD11 Macrophages

Heme oxygenase‐1 inhibits basophil maturation and activation but promotes its apoptosis in T helper type 2‐mediated allergic airway inflammation

Terminalia Chebulanin Attenuates Psoriatic Skin Lesion via Regulation of Heme Oxygenase-1

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