Nitrosative Stress as a Modulator of Inflammatory Change in a Model of Takotsubo Syndrome

Takotsubo syndrome reflects an ‘aberrant’ response to acute catecholamine stimulation, largely but not entirely as a manifestation of increased sensitivity to β‎2-adrenoceptor stimulation and signal transduction via Gi proteins, especially in ageing female hearts. It is now apparent that prolonged impairment of quality of life and slow recovery of echocardiographic parameters such as global longitudinal strain after episodes of takotsubo syndrome reflect ongoing myocardial inflammation and associated oedema, together with impairment of cardiac energetics on phosphorus magnetic resonance spectroscopy.

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Benzo(a)pyrene induce the inflammation, nitrosative stress and matrix degradation in articular cartilage

Bone Abstracts ◽

10.1530/boneabs.5.p211 ◽

2016 ◽

Author(s):

Tsung-Hsun Hsieh

Keyword(s):

Articular Cartilage ◽

Nitrosative Stress ◽

Matrix Degradation

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INFLAMMATORY BREAST CANCER FOLLOWED BY CONTRALATERAL BREAST METASTASIS WITH INFLAMMATORY CHANGE

The KITAKANTO Medical Journal ◽

10.2974/kmj1951.45.413 ◽

1995 ◽

Vol 45 (5) ◽

pp. 413-418

Author(s):

TATSUMASA ANDOH ◽

YUICHI IINO ◽

HIDETADA AOYAGI ◽

NORITAKA SUGAMATA ◽

HIROYUKI TAKEI ◽

...

Keyword(s):

Breast Cancer ◽

Inflammatory Breast Cancer ◽

Contralateral Breast ◽

Inflammatory Change ◽

Breast Metastasis

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Faculty Opinions recommendation of Exercise-induced oxidative-nitrosative stress is associated with impaired dynamic cerebral autoregulation and blood-brain barrier leakage.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.13165956.14503054 ◽

2011 ◽

Author(s):

Yves Jammes

Keyword(s):

Blood Brain Barrier ◽

Cerebral Autoregulation ◽

Nitrosative Stress ◽

Brain Barrier ◽

Blood Brain ◽

Exercise Induced ◽

Dynamic Cerebral Autoregulation

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Role of Heart Rate Reduction in the Management of Myocarditis

Current Pharmaceutical Design ◽

10.2174/1381612824666180111105923 ◽

2018 ◽

Vol 24 (3) ◽

pp. 365-378 ◽

Cited By ~ 2

Author(s):

Chen Guang-Yi ◽

Ge Li-Sha ◽

Li Yue-Chun

Keyword(s):

Heart Rate ◽

Nitrosative Stress ◽

Ventricular Remodeling ◽

Animal Experiments ◽

Viral Myocarditis ◽

Protective Effects ◽

Heart Rate Reduction ◽

Rate Reduction ◽

Beneficial Effects ◽

Biological Technique

The morbidity of myocarditis demonstrates an upward tendency by years, is commonly defined as the inflammation of myocytes and is caused by multiple factors. With the development of the molecular biological technique, great breakthroughs in the diagnosis and understanding of pathophysiological mechanisms of myocarditis have recently been achieved. Several questions remain unresolved, however, including standard treatment approaches to myocarditis, which remain controversial and ambiguous. Heart rate, as an independent risk factor, has been shown to be related to cardiac disease. Recent studies also show that the autonomic nervous system is involved in immunomodulatory myocarditis processes. Heart rate reduction treatment is recommended in myocarditis based on a number of animal experiments and clinical trials. It is possible that heart rate-lowering treatments can help to attenuate the inflammatory response and myocyte injury and reverse ventricular remodeling. However, how to execute the protective effects of heart rate reduction on myocarditis is still not clear. In this review, we discuss the pathogenesis and pathophysiological process of viral myocarditis and propose heart rate lowering as a therapeutic target for myocarditis, especially in light of the third-generation β-blockade carvedilol and funny channel blocker ivabradine. We also highlight some additional beneficial effects of such heart rate reduction agents, including anti-inflammatory, antioxidation, anti-nitrosative stress, anti-fibrosis and antiapoptosis properties.

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Melatonin As a Modulator of Degenerative and Regenerative Signaling Pathways in Injured Retinal Ganglion Cells

Current Pharmaceutical Design ◽

10.2174/1381612825666190829151314 ◽

2019 ◽

Vol 25 (28) ◽

pp. 3057-3073 ◽

Cited By ~ 6

Author(s):

Kobra B. Juybari ◽

Azam Hosseinzadeh ◽

Habib Ghaznavi ◽

Mahboobeh Kamali ◽

Ahad Sedaghat ◽

...

Keyword(s):

Optic Nerve ◽

Mitochondrial Dysfunction ◽

Signaling Pathways ◽

Retinal Ganglion Cells ◽

Molecular Mechanisms ◽

Nitrosative Stress ◽

Ganglion Cells ◽

Axon Growth ◽

Nerve Fibers ◽

Retinal Ganglion

Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance, etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including optic neuropathies. Based on the information provided in this review, melatonin may act as a promising agent to reduce RGC death in various retinal pathologic conditions.

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Myeloperoxidase-Related Chlorination Activity Is Positively Associated with Circulating Ceruloplasmin in Chronic Heart Failure Patients: Relationship with Neurohormonal, Inflammatory, and Nutritional Parameters

BioMed Research International ◽

10.1155/2015/691693 ◽

2015 ◽

Vol 2015 ◽

pp. 1-10 ◽

Cited By ~ 10

Author(s):

Aderville Cabassi ◽

Simone Maurizio Binno ◽

Stefano Tedeschi ◽

Gallia Graiani ◽

Cinzia Galizia ◽

...

Keyword(s):

Heart Failure ◽

Nitrosative Stress ◽

Defense Mechanism ◽

Nyha Class ◽

Protein Nitration ◽

Class Iii ◽

Oxidative And Nitrosative Stress ◽

Radical Production ◽

Antioxidant Function ◽

The Relationship

Rationale. Heart failure (HF) is accompanied by the development of an imbalance between oxygen- and nitric oxide-derived free radical production leading to protein nitration. Both chlorinating and peroxidase cycle of Myeloperoxidase (MPO) contribute to oxidative and nitrosative stress and are involved in tyrosine nitration of protein. Ceruloplasmin (Cp) has antioxidant function through its ferroxidase I (FeOxI) activity and has recently been proposed as a physiological defense mechanism against MPO inappropriate actions.Objective. We investigated the relationship between plasma MPO-related chlorinating activity, Cp and FeOxI, and nitrosative stress, inflammatory, neurohormonal, and nutritional biomarkers in HF patients.Methods and Results. In chronic HF patients (n=81, 76±9 years, NYHA Class II (26); Class III (29); Class IV (26)) and age-matched controls (n=17, 75±11 years, CTR), plasma MPO chlorinating activity, Cp, FeOxI, nitrated protein, free Malondialdehyde, BNP, norepinephrine, hsCRP, albumin, and prealbumin were measured. Plasma MPO chlorinating activity, Cp, BNP, norepinephrine, and hsCRP were increased in HF versus CTR. FeOxI, albumin, and prealbumin were decreased in HF. MPO-related chlorinating activity was positively related to Cp (r= 0.363,P<0.001), nitrated protein, hsCRP, and BNP and inversely to albumin.Conclusions. Plasma MPO chlorinated activity is increased in elderly chronic HF patients and positively associated with Cp, inflammatory, neurohormonal, and nitrosative parameters suggesting a role in HF progression.

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