Anti-inflammatory effect of ubiquinol-10 on young and senescent endothelial cells via miR-146a modulation

Olivieri, Fabiola; Lazzarini, Raffaella; Babini, Lucia; Prattichizzo, Francesco; Rippo, Maria Rita; Tiano, Luca; Nuzzo, Silvia; Graciotti, Laura; Festa, Roberto; Brugè, Francesca; Orlando, Patrick; Silvestri, Sonia; Capri, Miriam; Palma, Linda; Magnani, Mauro; Franceschi, Claudio; Littarru, Gian Paolo; Procopio, Antonio Domenico

doi:10.1016/j.freeradbiomed.2013.05.033

Cited by 67 publications

(60 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, ubiquinol is a particular molecule endowed with both antioxidant properties but also critical for mitochondrial bioenergetics. Recent reports have highlighted that differently from other antioxidants, ubiquinol is able to promote Nrf2 translocation and hence to increase positive stimuli following physical exercise, while inhibiting the NFkB inflammatory pathway [65,[73][74][75].…”

Section: Discussionmentioning

confidence: 99%

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

et al. 2018

Self Cite

View full text Add to dashboard Cite

Objectives: Physical exercise significantly impacts the biochemistry of the organism. Ubiquinone is a key component of the mitochondrial respiratory chain and ubiquinol, its reduced and active form, is an emerging molecule in sport nutrition. The aim of this study was to evaluate the effect of ubiquinol supplementation on biochemical and oxidative stress indexes after an intense bout of exercise. Methods: 21 male young athletes (26 + 5 years of age) were randomized in two groups according to a double blind cross-over study, either supplemented with ubiquinol (200 mg/day) or placebo for 1 month. Blood was withdrawn before and after a single bout of intense exercise (40 min run at 85% maxHR). Physical performance, hematochemical parameters, ubiquinone/ubiquinol plasma content, intracellular reactive oxygen species (ROS) level, mitochondrial membrane depolarization, paraoxonase activity and oxidative DNA damage were analyzed. Results: A single bout of intense exercise produced a significant increase in most hematochemical indexes, in particular CK and Mb while, on the contrary, normalized coenzyme Q 10 plasma content decreased significantly in all subjects. Ubiquinol supplementation prevented exercise-induced CoQ deprivation and decrease in paraoxonase activity. Moreover at a cellular level, in peripheral blood mononuclear cells, ubiquinol supplementation was associated with a significant decrease in cytosolic ROS while mitochondrial membrane potential and oxidative DNA damage remained unchanged. Discussion: Data highlights a very rapid dynamic of CoQ depletion following intense exercise underlying an increased demand by the organism. Ubiquinol supplementation minimized exerciseinduced depletion and enhanced plasma and cellular antioxidant levels but it was not able to improve physical performance indexes or markers of muscular damage.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

et al. 2018

Self Cite

View full text Add to dashboard Cite

show abstract

“…After age 40, mitochondrial capacity to reduce ubiquinone to ubiquinol progressively declines (Olivieri et al . ). Therefore, if an older individual experiences a TBI, there is less scavenging of ROS, resulting in greater cellular injury.…”

Section: Introductionmentioning

confidence: 97%

The use of antioxidants in the treatment of traumatic brain injury

Venegoni¹,

Shen

Thimmesch

et al. 2017

Journal of Advanced Nursing

View full text Add to dashboard Cite

Aims The aim of this study was to discuss secondary traumatic brain injury, the mitochondria and the use of antioxidants as a treatment. Background One of the leading causes of death globally is traumatic brain injury, affecting individuals in all demographics. Traumatic brain injury is produced by an external blunt force or penetration resulting in alterations in brain function or pathology. Often, with a traumatic brain injury, secondary injury causes additional damage to the brain tissue that can have further impact on recovery and the quality of life. Secondary injury occurs when metabolic and physiologic processes alter after initial injury and includes increased release of toxic free radicals that cause damage to adjacent tissues and can eventually lead to neuronal necrosis. Although antioxidants in the tissues can reduce free radical damage, the magnitude of increased free radicals overwhelms the body's reduced defence mechanisms. Supplementing the body's natural supply of antioxidants, such as coenzyme Q10, can attenuate oxidative damage caused by reactive oxygen species. Design Discussion paper. Data sources Research literature published from 2011–2016 in PubMed, CINAHL and Cochrane. Implications for nursing Prompt and accurate assessment of patients with traumatic brain injury by nurses is important to ensure optimal recovery and reduced lasting disability. Thus, it is imperative that nurses be knowledgeable about the secondary injury that occurs after a traumatic brain injury and aware of possible antioxidant treatments. Conclusion The use of antioxidants has potential to reduce the magnitude of secondary injury in patients who experience a traumatic brain injury.

show abstract

“…For example, miR-146a in cartilage has long been associated with osteoarthritis42. Moreover, under chronic inflammatory stimulation, miR-146a is overexpressed in different cell types, including endothelial cells and white blood cells [43]. High level of miR-146a was found in the blood of patients with coronary artery disease [24].…”

Section: Discussionmentioning

confidence: 99%

Toll-like 4 receptor /NFκB inflammatory/miR-146a pathway contributes to the ART-correlated preterm birth outcome

et al. 2016

View full text Add to dashboard Cite

Assisted reproductive technology (ART) is widely used for the women with infertility conditions to achieve pregnancy. However, the adverse effects of ART may lead to poor perinatal and neonatal outcomes, e.g., preterm birth and low body weight. In this study, we investigated the inflammatory molecular factors and microRNA that might be involved in ART related preterm birth. We found the elevation of Toll-like 4 receptor (TLR4), activation of NFκB pathway and down-regulation of microRNA-146a (miR-146a), a negative regulator of NFκB, in the placenta of preterm birth and ART, indicating preterm birth and ART were associated with inflammation signaling activation. In vitro experiments demonstrated that miR-146a suppressed NFκB pathway and shifted the balance of cytokines in the cord blood toward a repertoire of pro-inflammatory outcomes by down-regulating IRAK1 and TRAF6. The pro-inflammatory cytokines IL-6, IFNγ and TNFα in the cord blood were highly expressed in the preterm and ART, while anti-inflammatory cytokine IL-10 was the lower in the preterm and ART. In summary, we firstly uncovered that TLR4/NFκB mediated inflammation signaling and miR-146a participated in ART-related preterm birth patients, which suggests that importance of TLR4/NFκB/miR-146a signaling in clinical interventions and biomarkers of ART-related perinatal or neonatal outcomes.

show abstract

Anti-inflammatory effect of ubiquinol-10 on young and senescent endothelial cells via miR-146a modulation

Cited by 67 publications

References 48 publications

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes

The use of antioxidants in the treatment of traumatic brain injury

Toll-like 4 receptor /NFκB inflammatory/miR-146a pathway contributes to the ART-correlated preterm birth outcome

Contact Info

Product

Resources

About