scholarly journals Hydrogen Sulfide Attenuates Aortic Remodeling in Aortic Dissection Associating with Moderated Inflammation and Oxidative Stress through a NO-Dependent Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 682
Author(s):  
Hsin-Ying Lu ◽  
Hung-Lung Hsu ◽  
Chih-Han Li ◽  
Shao-Jung Li ◽  
Shing-Jong Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Inflammatory Response ◽  
Aortic Dissection ◽  
Vascular Remodeling ◽  
Aortic Wall ◽  
Inflammatory Cells ◽  
Sod Activity ◽  
Aortic Remodeling ◽  
And Oxidative Stress

Aortic dissection (AD) is a highly lethal vascular disease characterized by separation of the constituent layers of the aortic wall. An increasing body of research indicates that inflammatory response and oxidative stress are implicated in vascular remodeling, which plays a key role in the development of AD. Hydrogen sulfide (H2S) has been found to protect against various types of cardiovascular disease, including myocardial infarction, arthrosclerosis, and hypertension. However, research on the effect of H2S on AD is insufficient. This study therefore elucidated the effect of H2S on the development and progression of AD, and the potential mechanism involved. Using β-aminopropionitrile fumarate (BAPN) and angiotensin II (Ang-II)-induced AD animal models, the administration of NaHS (as H2S donor, 56 μmol/kg body weight/day) was found to retard the development of AD. Murine VSMCs (Movas) exposed to interleukin-6 (IL-6) (20 ng/mL) to induce phenotypic switch. Histological analyses indicated that H2S administration inhibited the accumulation of inflammatory cells in the aortic wall and the related expression of inflammatory genes. Additionally, H2S treatment elevated aortic superoxide dismutase (SOD) activity and ablated malonaldehyde (MDA) and nitric oxide (NO) levels. In mechanistic terms, H2S attenuated IL-6 induced a pathological VSMC phenotypical switch through NO modulation by N(G)-monomethyl-L-arginine acetate salt (L-NMMA) stimulation. H2S inhibits AD formation by decreasing the inflammatory response, and oxidative stress, and by positively participating in vascular remodeling. These findings suggest a role for H2S as a novel and promising therapeutic strategy to prevent AD development.

scholarly journals Astaxanthin protects cognitive function of vascular dementia

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Ningwei Zhu ◽  
Xiao Liang ◽  
Ming Zhang ◽  
Xiaolan Yin ◽  
Hui Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Function ◽  
Inflammatory Response ◽  
Vascular Dementia ◽  
Morris Water Maze Test ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dependent Manner ◽  
Sod Activity ◽  
Mda Content ◽  
And Oxidative Stress

Abstract Objective The purpose of this study was to evaluate the effect of astaxanthin (AST) on cognition function, inflammatory response and oxidative stress in vascular dementia (VD) mice. Method VD mice model was established by left unilateral common carotid arteries occlusion (LUCCAO). Following LUCCAO, AST was intragastrically administered for 30 days. Object recognition test and morris water maze test were used to evaluate cognitive function. Hematoxylin and eosin staining was performed to observe the hippocampal neuron structure. Enzyme-linked immunosorbent assay kit and bicinchoninic acid kit were respectively adopted to measure IL-1β and IL-4 protein expression and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in hippocampus and prefrontal cortex. Results AST improved the discrimination ability of VD mice. The escape latency and path length of VD mice treated with AST were dramatically reduced. Besides, AST 200 mg/kg enhanced crossing platform time and the number of times crossing the platform quadrant, and alleviated the morphological impairment in VD mice. Moreover, we found that AST inhibited IL-1β expression and MDA content, whereas promoted IL-4 expression and SOD activity in a dose-dependent manner. Conclusion AST could improve cognitive impairment and hippocampal neurons in VD mice, which may be related to suppression of inflammatory response and oxidative stress.

scholarly journals Inflammation and oxidative stress in vertebrate host–parasite systems

2008 ◽  
Vol 364 (1513) ◽  
pp. 71-83 ◽  
Author(s):  
Gabriele Sorci ◽  
Bruno Faivre
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Inflammatory Cells ◽  
Specific Response ◽  
Negative Effects ◽  
Short Term ◽  
Micro Organisms ◽  
Host Parasite ◽  
Benefits And Costs ◽  
And Oxidative Stress

Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms. Inflammation relies on a number of cellular and molecular effectors that can strike invading pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-specific way. Owing to this non-specific response, inflammation can generate substantial costs for the host if the inflammatory response, and the associated oxygen-based damage, get out of control. This imposes strong selection pressure that acts to optimize two key features of the inflammatory response: the timing of activation and resolution (the process of downregulation of the response). In this paper, we review the benefits and costs of inflammation-driven immunity. Our aim is to emphasize the importance of resolution of inflammation as a way of maintaining homeostasis against oxidative stress and to prevent the ‘horror autotoxicus’ of chronic inflammation. Nevertheless, host immune regulation also opens the way to pathogens to subvert host defences. Therefore, quantifying inflammatory costs requires assessing (i) short-term negative effects, (ii) delayed inflammation-driven diseases, and (iii) parasitic strategies to subvert inflammation.

scholarly journals Effects of hydrogen sulfide on hemodynamics, inflammatory response and oxidative stress during resuscitated hemorrhagic shock in rats

Critical Care ◽  
2010 ◽  
Vol 14 (5) ◽  
Author(s):  
Frédérique Ganster ◽  
Mélanie Burban ◽  
Mathilde de la Bourdonnaye ◽  
Lionel Fizanne ◽  
Olivier Douay ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Inflammatory Response ◽  
Hemorrhagic Shock ◽  
And Oxidative Stress

ACS67, a Hydrogen Sulfide–Releasing Derivative of Latanoprost Acid, Attenuates Retinal Ischemia and Oxidative Stress to RGC-5 Cells in Culture

2010 ◽  
Vol 51 (1) ◽  
pp. 284 ◽  
Author(s):  
Neville N. Osborne ◽  
Dan Ji ◽  
Aman S. Abdul Majid ◽  
Rebecca J. Fawcett ◽  
Anna Sparatore ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Retinal Ischemia ◽  
Cells In Culture ◽  
And Oxidative Stress

NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

RSC Advances ◽  
2016 ◽  
Vol 6 (69) ◽  
pp. 64208-64214 ◽  
Author(s):  
Shenglan Yang ◽  
Danfang Deng ◽  
Yingying Luo ◽  
Yanran Wu ◽  
Rui Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Irritable Bowel Syndrome ◽  
Hydrogen Sulfide ◽  
Murine Model ◽  
Irritable Bowel ◽  
And Oxidative Stress ◽  
Post Infectious

In this study, the alleviating role of hydrogen sulfide (H2S) was investigated in a Post-Infectious Irritable Bowel Syndrome (PI-IBS) murine model and Caco-2 cells.

MiR-22-3p Suppresses Vascular Remodeling and Oxidative Stress by Targeting CHD9 during the Development of Hypertension

2021 ◽  
pp. 1-11
Author(s):  
Hanqing Chen ◽  
Xiru Xu ◽  
Zhengqing Liu ◽  
Yong Wu
Keyword(s):  
Oxidative Stress ◽  
Vascular Remodeling ◽  
Underlying Mechanism ◽  
Inhibitory Effect ◽  
Spontaneously Hypertensive ◽  
Aortic Smooth Muscle ◽  
Phenotype Switch ◽  
And Oxidative Stress

Hypertension is considered a risk factor for a series of systematic diseases. Known factors including genetic predisposition, age, and diet habits are strongly associated with the initiation of hypertension. The current study aimed to investigate the role of miR-22-3p in hypertension. In this study, we discovered that the miR-22-3p level was significantly decreased in the thoracic aortic vascular tissues and aortic smooth muscle cells (ASMCs) of spontaneously hypertensive rats. Functionally, the overexpression of miR-22-3p facilitated the switch of ASMCs from the synthetic to contractile phenotype. To investigate the underlying mechanism, we predicted 11 potential target mRNAs for miR-22-3p. After screening, chromodomain helicase DNA-binding 9 (CHD9) was validated to bind with miR-22-3p. Rescue assays showed that the co-overexpression of miR-22-3p and CHD9 reversed the inhibitory effect of miR-22-3p mimics on cell proliferation, migration, and oxidative stress in ASMCs. Finally, miR-22-3p suppressed vascular remodeling and oxidative stress in vivo. Overall, miR-22-3p regulated ASMC phenotype switch by targeting CHD9. This new discovery provides a potential insight into hypertension treatment.

Cyane-carvone, a Synthetic Derivative of Carvone, Inhibits Inflammatory Response by Reducing Cytokine Production and Oxidative Stress and Shows Antinociceptive Effect in Mice

Inflammation ◽  
2014 ◽  
Author(s):  
Thiago Henrique Costa Marques ◽  
Maria Leonildes Boavista Gomes Cast Marques ◽  
Jand-Venes R. Medeiros ◽  
Renan Oliveira Silva ◽  
André Luiz dos Reis Barbosa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cytokine Production ◽  
Antinociceptive Effect ◽  
Synthetic Derivative ◽  
And Oxidative Stress
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