Toll-like receptor 7/8 agonist resiquimod induces late preconditioning in neonatal cardiac myocytes

Wang, Yong-Yi; Liu, Sha; Lin, Feng; Yang, Wengang; Xue, Song

doi:10.1038/aps.2011.6

Cited by 9 publications

(5 citation statements)

References 36 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Antioxidants, including vitamin E, can abrogate NF-κB activation [9,10]. Oxidation of p50 on its DNA-binding domain has been shown to act as a protective mechanism by preventing NF-κB binding [11]. Finally, a novel zinc-finger protein, MCPIP [MCP (monocyte chemoattractant protein)-1-induced protein], is thought to have NF-κB inhibitory activity in certain cell cultures, but its pathophysiological consequence in vivo remains undefined.…”

Section: Sources Of Rosmentioning

confidence: 99%

Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n−3 fatty acids: molecular mechanisms and potential clinical applications

2012

View full text Add to dashboard Cite

The role of oxidative stress in ischaemic heart disease has been thoroughly investigated in humans. Increased levels of ROS (reactive oxygen species) and RNS (reactive nitrogen species) have been demonstrated during ischaemia and post-ischaemic reperfusion in humans. Depending on their concentrations, these reactive species can act either as benevolent molecules that promote cell survival (at low-to-moderate concentrations) or can induce irreversible cellular damage and death (at high concentrations). Although high ROS levels can induce NF-κB (nuclear factor κB) activation, inflammation, apoptosis or necrosis, low-to-moderate levels can enhance the antioxidant response, via Nrf2 (nuclear factor-erythroid 2-related factor 2) activation. However, a clear definition of these concentration thresholds remains to be established. Although a number of experimental studies have demonstrated that oxidative stress plays a major role in heart ischaemia/reperfusion pathophysiology, controlled clinical trials have failed to prove the efficacy of antioxidants in acute or long-term treatments of ischaemic heart disease. Oral doses of vitamin C are not sufficient to promote ROS scavenging and only down-regulate their production via NADPH oxidase, a biological effect shared by vitamin E to abrogate oxidative stress. However, infusion of vitamin C at doses high enough to achieve plasma levels of 10 mmol/l should prevent superoxide production and the pathophysiological cascade of deleterious heart effects. In turn, n-3 PUFA (polyunsaturated fatty acid) exposure leads to enhanced activity of antioxidant enzymes. In the present review, we present evidence to support the molecular basis for a novel pharmacological strategy using these antioxidant vitamins plus n-3 PUFAs for cardioprotection in clinical settings, such as post-operative atrial fibrillation, percutaneous coronary intervention following acute myocardial infarction and other events that are associated with ischaemia/reperfusion.

show abstract

Section: Sources Of Rosmentioning

confidence: 99%

Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n−3 fatty acids: molecular mechanisms and potential clinical applications

2012

View full text Add to dashboard Cite

show abstract

“…Antioxidants, including vitamin E, can abrogate NF-κB activation. Oxidation of P50 on its DNA-binding domain has been shown to act as a protective mechanism by preventing NF-κB binding (Wang et al, 2011a ). Finally, a novel zinc-finger protein, monocyte chemoattractant protein-1 (MCP-1)-induced protein (MCPIP), is thought to have NF-κB inhibitory activity in certain cell cultures, but its pathophysiological consequence in vivo remains undefined.…”

Section: Implications Of Oxidative Stress For Heart Diseasementioning

confidence: 99%

Prevention of Postoperative Atrial Fibrillation: Novel and Safe Strategy Based on the Modulation of the Antioxidant System

Rodrigo¹

2012

Front. Physio.

View full text Add to dashboard Cite

Postoperative atrial fibrillation (AF) is the most common arrhythmia following cardiac surgery with extracorporeal circulation. The pathogenesis of postoperative AF is multifactorial. Oxidative stress, caused by the unavoidable ischemia–reperfusion event occurring in this setting, is a major contributory factor. Reactive oxygen species (ROS)-derived effects could result in lipid peroxidation, protein carbonylation, or DNA oxidation of cardiac tissue, thus leading to functional and structural myocardial remodeling. The vulnerability of myocardial tissue to the oxidative challenge is also dependent on the activity of the antioxidant system. High ROS levels, overwhelming this system, should result in deleterious cellular effects, such as the induction of necrosis, apoptosis, or autophagy. Nevertheless, tissue exposure to low to moderate ROS levels could trigger a survival response with a trend to reinforce the antioxidant defense system. Administration of n−3 polyunsaturated fatty acids (PUFA), known to involve a moderate ROS production, is consistent with a diminished vulnerability to the development of postoperative AF. Accordingly, supplementation of n−3 PUFA successfully reduced the incidence of postoperative AF after coronary bypass grafting. This response is due to an up-regulation of antioxidant enzymes, as shown in experimental models. In turn, non-enzymatic antioxidant reinforcement through vitamin C administration prior to cardiac surgery has also reduced the postoperative AF incidence. Therefore, it should be expected that a mixed therapy result in an improvement of the cardioprotective effect by modulating both components of the antioxidant system. We present novel available evidence supporting the hypothesis of an effective prevention of postoperative AF including a two-step therapeutic strategy: n−3 PUFA followed by vitamin C supplementation to patients scheduled for cardiac surgery with extracorporeal circulation. The present study should encourage the design of clinical trials aimed to test the efficacy of this strategy to offer new therapeutic opportunities to patients challenged by ischemia–reperfusion events not solely in heart, but also in other organs such as kidney or liver in transplantation surgeries.

show abstract

Section: Rational Use Of Oxidative Stress Preconditioningmentioning

confidence: 99%

“…The innate immune system is equipped with viral infection sensors and provides protective responses . The toll-like receptors (TLRs) and the RIG-I-like receptors (RLRs) play a dominant role in the initiation of subsequent adaptive and appropriate immunity such as T cell and B cell response. − Thus, targeting endogenous antiviral defense via the use of TLRs for their ability to recognize RNA viruses such as SARS-CoV-2 appears to be a suitable therapeutic approach against viral infection. , …”

Section: Rational Use Of Oxidative Stress Preconditioningmentioning

confidence: 99%

“…61−63 Thus, targeting endogenous antiviral defense via the use of TLRs for their ability to recognize RNA viruses such as SARS-CoV-2 appears to be a suitable therapeutic approach against viral infection. 64,65 RNA recognition by the innate immune system in response to viral infection is a key point for the initiation of immunity. 66 Hotz and colleagues showed that in vitro and in vivo preconditioning with a synthetic viral RNA (dsRNA), polyinosinic-polycytidylic acid [poly(I:C)], induced inhibition of RLRs and increased sensitivity of endosomal TLRs, in vitro via increased IFN-β and IL-12 signaling and in vivo through augmenting the activity of MAPK and NF-kB signaling pathways.…”

Section: Rational Use Of Oxidative Stressmentioning

confidence: 99%

See 1 more Smart Citation

COVID-19: Oxidative Preconditioning as a Potential Therapeutic Approach

Akki

Fath

Mohti

2020

ACS Chem. Neurosci.

View full text Add to dashboard Cite

This Article summarizes the likely benefits of central nervous system oxidative preconditioning in the reduction of COVID-19 based on its putative pathogenesis. The current COVID-19 outbreak caused a pandemic with millions of infected patients and death cases worldwide. The clinical features of severe acute respiratory syndrome coronavirus (SARS-CoV) was initially linked with respiratory disorders, but recent studies have reported alterations of neurological and cerebrovascular functions in COVID-19 patients. The main viral infection features are related to cell death, inflammation, and cytokine generation, which can be associated with the dysregulation of redox systems or oxidative stress. However, until now, there is no available and effective therapeutic approach. Thus, it is necessary to search for care and adequate protection against the disease, especially for susceptible and vulnerable groups. Preconditioning, a well-known antioxidative stress and anti-inflammatory approach, is protective against many neurological age-related disorders. COVID-19 severity and morbidity have been observed in elderly patients. The aim of the present study is to elucidate the possible protective role of oxidative preconditioning in aged patients at high risk of developing severe COVID-19 complications.

show abstract

Toll-like receptor 7/8 agonist resiquimod induces late preconditioning in neonatal cardiac myocytes

Cited by 9 publications

References 36 publications

Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n−3 fatty acids: molecular mechanisms and potential clinical applications

Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n−3 fatty acids: molecular mechanisms and potential clinical applications

Prevention of Postoperative Atrial Fibrillation: Novel and Safe Strategy Based on the Modulation of the Antioxidant System

COVID-19: Oxidative Preconditioning as a Potential Therapeutic Approach

Contact Info

Product

Resources

About