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

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.

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.

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

scholarly journals Lysophosphatidylcholine Offsets the Protective Effects of Bone Marrow Mesenchymal Stem Cells on Inflammatory Response and Oxidative Stress Injury of Retinal Endothelial Cells via TLR4/NF-κB Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Haijun Zhao ◽  
Yanhui He
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Inflammatory Response ◽  
Protective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury ◽  
Marrow Mesenchymal Stem Cells ◽  
And Oxidative Stress

Diabetic retinopathy (DR), as a major cause of blindness worldwide, is one common complication of diabetes mellitus. Inflammatory response and oxidative stress injury of endothelial cells play significant roles in the pathogenesis of DR. The study is aimed at investigating the effects of lysophosphatidylcholine (LPC) on the dysfunction of high glucose- (HG-) treated human retinal microvascular endothelial cells (HRMECs) after being cocultured with bone marrow mesenchymal stem cells (BMSCs) and the underlying regulatory mechanism. Coculture of BMSCs and HRMECs was performed in transwell chambers. The activities of antioxidant-related enzymes and molecules of oxidative stress injury and the contents of inflammatory cytokines were measured by ELISA. Flow cytometry analyzed the apoptosis of treated HRMECs. HRMECs were further treated with 10-50 μg/ml LPC to investigate the effect of LPC on the dysfunction of HRMECs. Western blotting was conducted to evaluate levels of TLR4 and p-NF-κB proteins. We found that BMSCs alleviated HG-induced inflammatory response and oxidative stress injury of HRMECs. Importantly, LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs. Furthermore, LPC upregulated the protein levels of TLR4 and p-NF-κB, activating the TLR4/NF-κB signaling pathway. Overall, our study demonstrated that LPC offsets the protective effects of BMSCs on inflammatory response and oxidative stress injury of HRMECs via TLR4/NF-κB signaling.

The investigation of the relationships of demodex density with inflammatory response and oxidative stress in rosacea

2018 ◽  
Vol 310 (9) ◽  
pp. 759-767 ◽  
Author(s):  
Tuğba Falay Gur ◽  
Aslı Vefa Erdemir ◽  
Mehmet Salih Gurel ◽  
Abdurrahim Kocyigit ◽  
Eray Metin Guler ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
And Oxidative Stress
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