scholarly journals Dose-dependent protective effect of nicotine in a murine model of viral myocarditis induced by coxsackievirus B3

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Ge Li-Sha ◽  
Zhao Jing-Lin ◽  
Chen Guang-Yi ◽  
Liu Li ◽  
Zhou De-Pu ◽  
...  
Keyword(s):  
Murine Model ◽  
Group Treatment ◽  
Inflammatory Diseases ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Left Ventricular ◽  
Untreated Group ◽  
Myocardial Inflammation ◽  
High Dose ◽  
Dose Dependent

Abstract The alpha 7 nicotinic acetylcholine receptor (alpha7 nAChR) was recently described as an anti-inflammatory target in various inflammatory diseases. The aim of this study was to investigate the dose-related effects of nicotine, an alpha7 nAChR agonist, in murine model of viral myocarditis. BALB/C mice were infected by an intraperitoneally injection with coxsackievirus B3. Nicotine was administered at doses of 0.1, 0.2 or 0.4 mg/kg three times per day for 7 or 14 consecutive days. The effects of nicotine on survival, myocardial histopathological changes, cardiac function and cytokine levels were studied. The survival rate on day 14 increased in a dose-dependent fashion and was markedly higher in the 0.2 and 0.4 mg/kg nicotine groups than in the infected untreated group. Treatment with high-dose nicotine reduced the myocardial inflammation and improved the impaired left ventricular function in infected mice. The mRNA expressions and protein levels of TNF-α, IL-1β, IL-6 and IL-17A were significantly downregulated in dose-dependent manners in the nicotine treatment groups compared to the infected untreated group. Nicotine dose-dependently reduced the severity of viral myocarditis through inhibiting the production of proinflammatory cytokines. The findings suggest that alpha7 nAChR agonists may be a promising new strategy for patients with viral myocarditis.

scholarly journals Erratum: Dose-dependent protective effect of nicotine in a murine model of viral myocarditis induced by coxsackievirus B3

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Ge Li-Sha ◽  
Zhao Jing-Lin ◽  
Chen Guang-Yi ◽  
Liu Li ◽  
Zhou De-Pu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Murine Model ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Dose Dependent

scholarly journals Dapagliflozin Alleviates Myocardial Inflammation by Regulating the Macrophage Polarization and Stat3-related Pathways in Coxsackie Virus B3-induced Acute Viral Myocarditis

2022 ◽  
Author(s):  
Pengcheng Yan ◽  
Xiaoning Song ◽  
Joanne Tran ◽  
Runfa Zhou ◽  
Xinran Cao ◽  
...  
Keyword(s):  
Cardiac Tissue ◽  
Inflammatory Diseases ◽  
Macrophage Polarization ◽  
Viral Myocarditis ◽  
Coxsackie Virus ◽  
Myocardial Inflammation ◽  
Protective Effects ◽  
Acute Viral Myocarditis ◽  
Cvb3 Infection ◽  
Coxsackie Virus B3

Abstract Viral myocarditis (VMC), which is most prevalently caused by Coxsackievirus B3 (CVB3) infection, is a serious clinical condition characterized by cardiac inflammation. Dapagliflozin, a kind of sodium glucose co-transporters 2(SGLT-2) inhibitor, exhibited protective effects on plenty of inflammatory diseases, while its effect on viral myocarditis has not been studied. Recently we found the protective effect of dapagliflozin on VMC. After CVB3 infection, dapagliflozin were given orally to Balb/c male mice for 8 days and then the severity of myocarditis was assessed. Our results indicated that dapagliflozin significantly alleviated the severity of viral myocarditis, elevated the survival rate, and ameliorated cardiac function. Besides, dapagliflozin can decrease the level of proinflammatory cytokines included IL-1β, IL-6, TNF-α. Furthermore, dapagliflozin can inhibit macrophages differentiate to classically activated macrophages (M1) in cardiac tissue and activate the Stat3 signal pathway which is reported to promote polarization of the alternatively activated macrophage (M2). In conclusion, our study demonstrates that dapagliflozin alleviates myocardial inflammation by regulating the macrophage polarization and Stat3-related pathways in coxsackie virus B3-induced acute viral myocarditis.

scholarly journals Comparison of Effects of Ivabradine versus Carvedilol in Murine Model with the Coxsackievirus B3-Induced Viral Myocarditis

PLoS ONE ◽  
2012 ◽  
Vol 7 (6) ◽  
pp. e39394 ◽  
Author(s):  
Li Yue-Chun ◽  
Zhang Teng ◽  
Zhou Na-Dan ◽  
Ge Li-Sha ◽  
Luo Qin ◽  
...  
Keyword(s):  
Murine Model ◽  
Viral Myocarditis ◽  
Coxsackievirus B3

scholarly journals Effects of “Danzhi Decoction” on Chronic Pelvic Pain, Hemodynamics, and Proinflammatory Factors in the Murine Model of Sequelae of Pelvic Inflammatory Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaoling Bu ◽  
Yanxia Liu ◽  
Qiudan Lu ◽  
Zhe Jin
Keyword(s):  
Pelvic Pain ◽  
Murine Model ◽  
Genital Tract ◽  
Chronic Pelvic Pain ◽  
Inflammatory Diseases ◽  
Blood Stasis ◽  
High Dose ◽  
Positive Role ◽  
Blood Flows ◽  
Proinflammatory Factors

Objective.To evaluate the effect of Danzhi decoction (DZD) on chronic pelvic pain (CPP), hemodynamics, and proinflammatory factors of sequelae of pelvic inflammatory diseases (SPID) in murine model.Methods.SPID mice were randomly treated with high-dose DZD, mid-dose DZD, low-dose DZD, aspirin, and vehicle for 3 estrous circles. The Mouse Grimace Scale (MGS) was performed to evaluate CPP; blood flows of the upper genital tract, pelvic wall, and mesentery were used to assess hemodynamics in SPID mice; expressions of vascular endothelial growth factor (VEGF), angiopoietin-2 (Ang-2), and osteopontin (OPN) were measured by Western blot and immunochemistry.Results.Treatment with dose-dependent DZD significantly decreased the MGS scores, accelerated blood flows of the pelvis, and reduced expressions of VEGF, Ang-2, and OPN in the upper genital tract.Conclusions and Discussions.DZD was effective in relieving CPP and improving hemodynamics of the pelvic blood-stasis microenvironment in SPID mice. There was a relationship between CPP and the pelvic blood-stasis microenvironment. Furthermore, DZD might play a positive role in the anti-inflammatory process.

scholarly journals Astragaloside IV reduces cardiomyocyte apoptosis in a murine model of coxsackievirus B3-induced viral myocarditis

2019 ◽  
Vol 68 (4) ◽  
pp. 549-558 ◽  
Author(s):  
Tianlong Liu ◽  
Fan Yang ◽  
Jing Liu ◽  
Mingjie Zhang ◽  
Jianjun Sun ◽  
...  
Keyword(s):  
Murine Model ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Cardiomyocyte Apoptosis ◽  
Astragaloside Iv

scholarly journals Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

Biology ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 335
Author(s):  
Kathleen Pappritz ◽  
Sophie Van Linthout
Keyword(s):  
Immune System ◽  
Severe Disease ◽  
Treatment Options ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Specific Model ◽  
Left Ventricular ◽  
Inflammatory Disorder ◽  
Inflammatory Models ◽  
The Impact

Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The pathogenesis of viral myocarditis is conceptually a multiphase process, initiated by the infection of cardiomyocytes, followed by activation of the immune system, and resulting in myocardial fibrosis and left ventricular dysfunction. In parallel to the direct infection of the heart, CVB3 replicates in lymphatic organs such as the pancreas. Due to infection of the pancreas, the model of experimental CVB3-induced myocarditis is estimated as a severe burden for the challenged animals. Application of analgesics in frame of the animal welfare act (European directive 2010/63/EU) is more and more becoming a matter of debate. For this purpose, we summarized published studies for 13 different opioids and discussed their potential impact on CVB3-induced myocarditis. In addition, with this summary we also want to provide guidance for researchers beyond the myocarditis field to estimate the impact of opioids on the immune system for their specific model. In the literature, both immunosuppressive as well as immune-activating effects of opioids have been described, but examinations in experimental CVB3-induced myocarditis have still not been reported so far. Based on the existing publications, administration of opioids in experimental CVB3-induced myocarditis might result in more severe disease progression, including higher mortality, or a less pronounced myocarditis model, failing to be used for the establishment of new treatment options. Taken together, the applicability of opioids in experimental CVB3-induced myocarditis and in inflammatory models in general needs to be carefully evaluated and further investigated.

scholarly journals Early Evidence of Cardiotoxicity and Tumor Response in Patients with Sarcomas after High Cumulative Dose Doxorubicin Given as a Continuous Infusion

Sarcoma ◽  
2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Raymundo A. Quintana ◽  
Jose Banchs ◽  
Ridhi Gupta ◽  
Heather Y. Lin ◽  
Sean D. Raj ◽  
...  
Keyword(s):  
Continuous Infusion ◽  
Cumulative Dose ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
High Dose ◽  
Disease Group ◽  
Ventricular Ejection Fraction ◽  
Early Evidence ◽  
High Cumulative Dose ◽  
Dose Dependent

Background. Despite the dose-dependent response rate of sarcomas to doxorubicin, clinicians limit its cumulative dose due to cardiotoxicity. This study evaluates early evidence of cardiotoxicity in patients treated with high-dose doxorubicin given as a continuous infusion. Methods. Data was collected on patients who received 90 mg/m2 doxorubicin as a continuous infusion and 10 gm/m2 ifosfamide for up to 6 cycles as part of a phase II study. Cardiotoxicity was assessed with serial echocardiograms or multigated acquisition scans and serum brain natriuretic peptide and troponin levels. Tumor responses were determined by serial radiographic imaging per RECIST. Result. Out of the 48 patients enrolled, no patient developed heart failure symptoms; however, 4 out of the 38 (10%) patients with serial left ventricular ejection fraction assessments developed subclinical cardiotoxicity (asymptomatic drop in LVEF ≥ 10%). Twenty-three patients received all six 72-hour cycles of doxorubicin with a mean cumulative dose of 540 mg/m2. Among these patients, 4% (n=1) developed subclinical cardiotoxicity. In the advanced disease group (n=39), patients with a complete or partial response received a higher mean cumulative dose than those with stable disease (p<0.033). Conclusions. Doxorubicin cardiotoxicity can be limited by administering doxorubicin as a continuous infusion, allowing higher cumulative dosing to maximize efficacy.

Protective Effects of Carvedilol in Murine Model With the Coxsackievirus B3-Induced Viral Myocarditis

2008 ◽  
Vol 51 (1) ◽  
pp. 92-98 ◽  
Author(s):  
Li Yue-Chun ◽  
Ge Li-Sha ◽  
Ren Jiang-Hua ◽  
Yang Peng-Lin ◽  
Lin Jia-Feng ◽  
...  
Keyword(s):  
Murine Model ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Protective Effects

Carvedilol has stronger anti-inflammation and anti-virus effects than metoprolol in murine model with coxsackievirus B3-induced viral myocarditis

Gene ◽  
2014 ◽  
Vol 547 (2) ◽  
pp. 195-201 ◽  
Author(s):  
Dan Wang ◽  
Yiming Chen ◽  
Jianbin Jiang ◽  
Aihua Zhou ◽  
Lulu Pan ◽  
...  
Keyword(s):  
Murine Model ◽  
Viral Myocarditis ◽  
Coxsackievirus B3 ◽  
Anti Inflammation
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