Exercise in systemic sclerosis intensifies systemic inflammation and oxidative stress

2010 ◽  
Vol 39 (1) ◽  
pp. 63-70 ◽  
Author(s):  
H Harðardóttir ◽  
HAC van Helvoort ◽  
MC Vonk ◽  
FHJ van den Hoogen ◽  
PNR Dekhuijzen ◽  
...  
BioFactors ◽  
2021 ◽  
Author(s):  
Fatemeh Amin ◽  
Arghavan Memarzia ◽  
Hamideh Kazemi Rad ◽  
Farzaneh Shakeri ◽  
Mohammad Hossein Boskabady

Author(s):  
Marco Orlandi ◽  
Stefano Masi ◽  
Devina Bhowruth ◽  
Yago Leira ◽  
Georgios Georgiopoulos ◽  
...  

Objective: Inflammation, oxidative stress, and endothelial dysfunction are known to contribute to ischemia-reperfusion injury. Remote ischemic preconditioning (RIPC) protects from endothelial dysfunction and the damage induced by ischemia-reperfusion. Using intensive periodontal treatment (IPT), an established human model of acute systemic inflammation, we investigated whether RIPC prevents endothelial dysfunction and modulates systemic levels of inflammation and oxidative stress. Approach and Results: Forty-nine participants with periodontitis were randomly allocated to receive either 3 cycles of ischemia-reperfusion on the upper limb (N=25, RIPC) or a sham procedure (N=24, control) before IPT. Endothelial function assessed by flow-mediated dilatation of the brachial artery, inflammatory cytokines, markers of vascular injury, and oxidative stress were evaluated at baseline, day 1, and day 7 after IPT. Twenty-four hours post-IPT, the RIPC group had lower levels of IL (interleukin)-10 and IL-12 compared with the control group ( P <0.05). RIPC attenuated the IPT-induced increase in IL-1β, E-selectin, sICAM-3 (soluble intercellular adhesion molecule 3), and s-thrombomodulin levels between the baseline and day 1 ( P for interaction <0.1). Conversely, oxidative stress was differentially increased at day1 in the RIPC group compared with the control group ( P for interaction <0.1). This was accompanied by a better flow-mediated dilatation (mean difference 1.75% [95% CI, 0.428–3.07], P =0.011). After 7 days from IPT, most of the inflammatory markers endothelial-dependent and -independent vasodilation were similar between groups. Conclusions: RIPC prevented acute endothelial dysfunction by modulation of inflammation and oxidation processes in patients with periodontitis following exposure to an acute inflammatory stimulus. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03072342.


2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Aluisio Andrade-Lima ◽  
Natan da Silva Junior ◽  
Marcel Chehuen ◽  
Roberto Miyasato ◽  
Rodrigo W.A. Souza ◽  
...  

2018 ◽  
Vol 15 (1) ◽  
Author(s):  
Joana Costa d’Avila ◽  
Luciana Domett Siqueira ◽  
Aurélien Mazeraud ◽  
Estefania Pereira Azevedo ◽  
Debora Foguel ◽  
...  

2016 ◽  
Vol 130 (13) ◽  
pp. 1039-1050 ◽  
Author(s):  
Victoria Austin ◽  
Peter J. Crack ◽  
Steven Bozinovski ◽  
Alyson A. Miller ◽  
Ross Vlahos

Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and loss of lung function, and is currently the third largest cause of death in the world. It is now well established that cardiovascular-related comorbidities such as stroke contribute to morbidity and mortality in COPD. The mechanisms linking COPD and stroke remain to be fully defined but are likely to be interconnected. The association between COPD and stroke may be largely dependent on shared risk factors such as aging and smoking, or the association of COPD with traditional stroke risk factors. In addition, we propose that COPD-related systemic inflammation and oxidative stress may play important roles by promoting cerebral vascular dysfunction and platelet hyperactivity. In this review, we briefly discuss the pathogenesis of COPD, acute exacerbations of COPD (AECOPD) and cardiovascular comorbidities associated with COPD, in particular stroke. We also highlight and discuss the potential mechanisms underpinning the link between COPD and stroke, with a particular focus on the roles of systemic inflammation and oxidative stress.


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