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      Chitoheptaose Promotes Heart Rehabilitation in a Rat Myocarditis Model by Improving Antioxidant, Anti-Inflammatory, and Antiapoptotic Properties

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          Abstract

          Background

          Myocarditis is one of the important causes of dilated cardiomyopathy, cardiac morbidity, and mortality worldwide. Chitosan oligosaccharides (COS) may have anti-inflammatory and cardioprotective effects on myocarditis. However, the exact molecular mechanism for the effects of functional COS on myocarditis remains unclear.

          Methods

          Anti-inflammatory activities of COS (chitobiose, chitotriose, chitotetraose, chitopentaose, chitohexaose, chitoheptaose, and chitooctaose) were measured in lipopolysaccharide- (LPS-) stimulated RAW264.7 cells. A rat model with myocarditis was established and treated with chitopentaose, chitohexaose, chitoheptaose, and chitooctaose. Serum COS were measured by using high-performance liquid chromatography (HPLC) in all rats. Myocarditis injury, the levels of reactive oxygen species (ROS), reactive nitrogen species (RNS), inflammatory factors, and apoptotic factors were also measured. Pearson's correlation coefficient test was used to explore the relationship between the levels of ROS/RNS and cardiac parameters.

          Results

          Among all chitosan oligosaccharides, the COS > degrees of polymerization (DP) 4 showed anti-inflammatory activities (the activity order was chitopentaose<chitohexaose<chitoheptaose<chitooctaose) by reducing the levels of interleukin- (IL-) 1 β, IL-17A, and interferon- (IFN-) γ and increasing the level of IL-10. However, the serum level of chitooctaose was low whereas it showed significant therapeutic effects on myocarditis by improving cardiac parameters (left ventricular internal dimension, both end-systolic and end-diastolic, ejection fraction, and fractional shortening), inflammatory cytokines (IL-1 β, IL-10, IL-17A, and IFN- γ), oxidative factors (ROS and RNS), and apoptotic factors (caspase 3, BAX, and BCL-2) when compared with chitopentaose, chitohexaose, and chitooctaose (COS DP > 4). The levels of ROS/RNS had a strong relationship with cardiac parameters.

          Conclusions

          Chitoheptaose plays a myriad of cardioprotective roles in the myocarditis model via its antioxidant, anti-inflammatory, and antiapoptotic activities.

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          IL-12 receptor beta 1 and Toll-like receptor 4 increase IL-1 beta- and IL-18-associated myocarditis and coxsackievirus replication.

          Susan Yusung, DeLisa Fairweather, Sylvia Frisancho-Kiss … (2003)
          Th1-type immune responses, mediated by IL-12-induced IFN-gamma, protect the host from most viral infections. To investigate the role of IL-12 and IFN-gamma on the development of Coxsackievirus B3 (CB3)-induced myocarditis, we examined the level of inflammation, viral replication, and cytokine production in IL-12Rbeta1- and IFN-gamma-deficient mice following CB3 infection. We report that IL-12Rbeta1 deficiency results in decreased viral replication and inflammation in the heart, while IFN-gamma deficiency exacerbates CB3 replication. Importantly, decreased IL-1beta and IL-18 levels in IL-12Rbeta1-deficient hearts correlated directly with decreased myocardial inflammation. Because IL-1beta and IL-18 were associated with myocardial inflammation, we examined the effect of TLR4 deficiency on CB3 infection and myocarditis. We found that TLR4-deficient mice also had significantly reduced levels of myocarditis, viral replication, and IL-1beta/IL-18, just as we had observed in IL-12Rbeta1-deficient mice. This is the first report that TLR4 influences CB3 replication. These results show that IL-12Rbeta1 and TLR4 exacerbate CB3 infection and myocarditis while IFN-gamma protects against viral replication. The remarkable similarities between the effects of IL-12Rbeta1 and TLR4 suggest that these receptors share common downstream pathways that directly influence IL-1beta and IL-18 production, and confirm that IL-1beta and IL-18 play a significant role in the pathogenesis of CB3-induced myocarditis. These findings have important implications not only for the pathogenesis of myocarditis, but for other autoimmune diseases triggered by viral infections.
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            IL‐1 receptor antagonist, anakinra, prevents myocardial dysfunction in a mouse model of Kawasaki disease vasculitis and myocarditis

            M. Gorelik, Y. Lee, M. Abe … (2019)
            Summary Kawasaki disease (KD) vasculitis is an acute febrile illness of childhood characterized by systemic vasculitis of unknown origin, and is the most common cause of acquired heart disease among children in the United States. While  histological evidence of myocarditis can be found in all patients with acute KD, only a minority of patients are clinically symptomatic and a subset demonstrate echocardiographic evidence of impaired myocardial function, as well as increased left ventricular mass, presumed to be due to myocardial edema and inflammation. Up to a third of KD patients fail to respond to first‐line therapy with intravenous immunoglobulin (IVIG), and the use of interleukin (IL)‐1 receptor antagonist (IL‐1Ra, anakinra) is currently being investigated as an alternative therapeutic approach to treat IVIG‐resistant patients. In this study, we sought to investigate the effect of IL‐1Ra on myocardial dysfunction and its relation to myocarditis development during KD vasculitis. We used the Lactobacillus casei cell‐wall extract (LCWE)‐induced murine model of KD vasculitis and investigated the effect of IL‐1Ra pretreatment on myocardial dysfunction during KD vasculitis by performing histological, magnetic resonance imaging (MRI) and echocardiographic evaluations. IL‐1Ra pretreatment significantly reduced KD‐induced myocardial inflammation and N‐terminal pro B‐type natriuretic peptide (NT‐proBNP) release. Both MRI and echocardiographic studies on LCWE‐injected KD mice demonstrated that IL‐1Ra pretreatment results in an improved ejection fraction and a normalized left ventricular function. These findings further support the potential beneficial effects of IL‐1Ra therapy in preventing the cardiovascular complications in acute KD patients, including the myocarditis and myocardial dysfunction associated with acute KD.
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              Involvement of Nrf2-mediated heme oxygenase-1 expression in anti-inflammatory action of chitosan oligosaccharides through MAPK activation in murine macrophages.

              Jun-Ho Hyung, Chang-Bum Ahn, Boo Il Kim … (2016)
              Chitosan and its derivatives have been reported to have anti-inflammatory effects in vitro and in vivo. It is also suggested that chitosan and its derivatives could be up-regulating heme oxygenase-1 (HO-1) in different models. However, the up-regulation of HO-1 by chitosan oligosaccharides (COS) remains unexplored in regard to anti-inflammatory action in lipopolysaccharide (LPS)-stimulated murine macrophages (RAW264.7 cells). Treatment with COS induced HO-1 expression in LPS-stimulated RAW264.7 cells, whereas the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was decreased. Pretreatment with ZnPP, a HO-1 inhibitor, reduced the COS-mediated anti-inflammatory action. HO-1 induction is mediated by activating the nuclear translocation of NF-E2-related factor 2 (Nrf2) using COS. Moreover, COS increased the phosphorylation of extracellular signal regulated kinase (ERK1/2), c-Jun N-terminal kinase/stress-activated protein kinase (JNK), and p38 MAPK. However, specific inhibitors of ERK, JNK, and p38 reduced COS-mediated nuclear translocation of Nrf2. Therefore, HO-1 induction also decreased in RAW264.7 cells. Collectively, COS exert an anti-inflammatory effect through Nrf2/MAPK-mediated HO-1 induction.
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                Author and article information

                Contributors
                Long Liu:
                ORCID: https://orcid.org/0000-0003-1640-6980
                Hong Ji:
                ORCID: https://orcid.org/0000-0003-1776-8756
                Journal
                Journal ID (nlm-ta): Oxid Med Cell Longev
                Journal ID (iso-abbrev): Oxid Med Cell Longev
                Journal ID (publisher-id): OMCL
                Title: Oxidative Medicine and Cellular Longevity
                Publisher: Hindawi
                ISSN (Print): 1942-0900
                ISSN (Electronic): 1942-0994
                Publication date Collection: 2020
                Publication date (Electronic): 11 April 2020
                Volume: 2020
                Electronic Location Identifier: 2394704
                Affiliations
                1Department of Cardiovascular Medicine, The Third Hospital of Jilin Unversity, Changchun 130033, China
                2Jilin Provincial Precision Medicine Key Laboratory for Cardiovascular Genetic Diagnosis, Changchun 130033, China
                3Rehabilitation Medicine Department, The Third Hospital of Jilin Unversity, Changchun 130033, China
                4Department of Pathology, The Third Hospital of Jilin Unversity, Changchun 130033, China
                5Department of Pharmacy, The Third Hospital of Jilin Unversity, Changchun 130033, China
                Author notes

                Guest Editor: Mansur A. Sandhu

                Author information
                https://orcid.org/0000-0003-1640-6980
                https://orcid.org/0000-0003-1776-8756
                Article
                DOI: 10.1155/2020/2394704
                PMC ID: 7171680
                PubMed ID: 32351668
                SO-VID: f074dd70-6736-40da-a88f-e047d6741605
                Copyright © Copyright © 2020 Qini Zhao et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 13 January 2020
                Date revision received : 12 February 2020
                Date accepted : 24 February 2020
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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