Hydroxytyrosol improves strenuous exercise-associated cardiac pathological changes<i>via</i>modulation of mitochondrial homeostasis

Xu, Jie; Cao, Wei; Zhang, Jiawei; Feng, Zhihui; Cao, Ke

doi:10.1039/d2fo00839d

Cited by 4 publications

(3 citation statements)

References 44 publications

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“…No genotoxicity of HT has been reported in humans, and multiple benefits have been revealed in the past decades through extensive studies [36]. We previously reported that HT could prevent diet-induced metabolic syndrome [37] and improve strenuous exercise-associated cardiac pathological changes [38] as well as protecting RPE cells against oxidative stress via activating Nrf2 signaling [17]. Other phenol compounds such as tyrosol and oleuropein have also been reported to activate Nrf2 for the protection of cellular stress and damage [39,40].…”

Section: Discussionmentioning

confidence: 99%

Comparative Study of Hydroxytyrosol Acetate and Hydroxytyrosol in Activating Phase II Enzymes

Zou,

Zeng,

Zheng

et al. 2023

Antioxidants

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Nuclear factor E2-related factor 2 (Nrf2) is fundamental to the maintenance of redox homeostasis within cells via the regulation of a series of phase II antioxidant enzymes. The unique olive-derived phenolic compound hydroxytyrosol (HT) is recognized as an Nrf2 activator, but knowledge of the HT derivative hydroxytyrosol acetate (HTac) on Nrf2 activation remains limited. In this study, we observed that an HT pretreatment could protect the cell viability, mitochondrial membrane potential, and redox homeostasis of ARPE-19 cells against a t-butyl hydroperoxide challenge at 50 μM. HTac exhibited similar benefits at 10 μM, indicating a more effective antioxidative capacity compared with HT. HTac consistently and more efficiently activated the expression of Nrf2-regulated phase II enzymes than HT. PI3K/Akt was the key pathway accounting for the beneficial effects of HTac in ARPE-19 cells. A further RNA-Seq analysis revealed that in addition to the consistent upregulation of phase II enzymes, the cells presented distinct expression profiles after HTac and HT treatments. This indicated that HTac could trigger a diverse cellular response despite its similar molecular structure to HT. The evidence in this study suggests that Nrf2 activation is the major cellular activity shared by HTac and HT, and HTac is more efficient at activating the Nrf2 system. This supports its potential future employment in various disease management strategies.

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Section: Discussionmentioning

confidence: 99%

Comparative Study of Hydroxytyrosol Acetate and Hydroxytyrosol in Activating Phase II Enzymes

Zou,

Zeng,

Zheng

et al. 2023

Antioxidants

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“…EE decreases the number of myocardial mitochondria and the mass of the myocardium by downregulating Mfn2 and increasing Drp1, resulting in energy metabolism imbalance and myocardial damage. In addition, the expression of Mfn1 and OPA1 was not affected by EE (37,54). Another study illustrated that phosphorylation of Drp1, but not Drp1, affects mitochondrial fission during EE.…”

Section: Figurementioning

confidence: 98%

“…Knockdown of PGC-1α may cause stalled mitochondrial turnover and death in cardiomyocytes, thereby affecting cardiac function and leading to a reduction in exercise-induced metabolic benefits (36). EE leads to a marked downregulation of PGC-1α and mitochondrial respiratory chain complexes I and II in the heart, along with a reduction in mtDNA copy number (37). A drop in mitochondrial complex I and II activity would suppress mitochondrial oxidative phosphorylation and increase ROS yield.…”

Section: Role Of Mitochondrial Biogenesis In Ee-induced Myocardial In...mentioning

confidence: 99%

Novel insights into exhaustive exercise-induced myocardial injury: Focusing on mitochondrial quality control

Shi

Zhang

Zhao

et al. 2022

Front. Cardiovasc. Med.

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Regular moderate-intensity exercise elicits benefit cardiovascular health outcomes. However, exhaustive exercise (EE) triggers arrhythmia, heart failure, and sudden cardiac death. Therefore, a better understanding of unfavorable heart sequelae of EE is important. Various mechanisms have been postulated for EE-induced cardiac injury, among which mitochondrial dysfunction is considered the cardinal machinery for pathogenesis of various diseases. Mitochondrial quality control (MQC) is critical for clearance of long-lived or damaged mitochondria, regulation of energy metabolism and cell apoptosis, maintenance of cardiac homeostasis and alleviation of EE-induced injury. In this review, we will focus on MQC mechanisms and propose mitochondrial pathophysiological targets for the management of EE-induced myocardial injury. A thorough understanding of how MQC system functions in the maintenance of mitochondrial homeostasis will provide a feasible rationale for developing potential therapeutic interventions for EE-induced injury.

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Anti-oxidant and Anti-ageing Mechanism of Bioactive Compounds in Modulating the Ageing-Related Epigenetic Factors

Das

Dey

Duttaroy

et al. 2023

Evidence-Based Functional Foods for Prevention of Age-Related Diseases

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Hydroxytyrosol improves strenuous exercise-associated cardiac pathological changesviamodulation of mitochondrial homeostasis

Abstract: Hydroxytyrosol (HT) from olive oil exerts profitable effects on strenuous exercise-induced cardiac pathological changes via modulation of mitochondrial homeostasis.

Cited by 4 publications

References 44 publications

Comparative Study of Hydroxytyrosol Acetate and Hydroxytyrosol in Activating Phase II Enzymes

Comparative Study of Hydroxytyrosol Acetate and Hydroxytyrosol in Activating Phase II Enzymes

Novel insights into exhaustive exercise-induced myocardial injury: Focusing on mitochondrial quality control

Anti-oxidant and Anti-ageing Mechanism of Bioactive Compounds in Modulating the Ageing-Related Epigenetic Factors

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