Inhibition of MEK/ERK/STAT3 signaling in oleuropein treatment inhibits myocardial ischemia/reperfusion

Jin, Hongxu; Zhang, Yun‐Hu; Guo, Ruo‐Nan; Zhao, Su‐Nuan

doi:10.3892/ijmm.2018.3673

Cited by 17 publications

(22 citation statements)

References 32 publications

(40 reference statements)

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“…Recent study suggested protective effect of Ole on myocardial ischemia/reperfusion in neonatal rat cardiomyocytes due to inhibition of apoptosis [201]. Also, Ole inhibited myocardial infarction size and decreased creatinine kinase-MB and LDH serum levels in a myocardial ischemia/reperfusion rat model [202]. Furthermore, it was shown that Ole exerts cardioprotection in cholesterol-fed animals through activation of intracellular signaling, reduces the circulating cholesterol and LDL levels and increases myocardial ATP content [203].…”

Section: Oleuropeinmentioning

confidence: 99%

Hydroxytyrosol, Tyrosol and Derivatives and Their Potential Effects on Human Health

et al. 2019

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The Mediterranean diet and olive oil as its quintessential part are almost synonymous with a healthy way of eating and living nowadays. This kind of diet has been highly appreciated and is widely recognized for being associated with many favorable effects, such as reduced incidence of different chronic diseases and prolonged longevity. Although olive oil polyphenols present a minor fraction in the composition of olive oil, they seem to be of great importance when it comes to the health benefits, and interest in their biological and potential therapeutic effects is huge. There is a growing body of in vitro and in vivo studies, as well as intervention-based clinical trials, revealing new aspects of already known and many new, previously unknown activities and health effects of these compounds. This review summarizes recent findings regarding biological activities, metabolism and bioavailability of the major olive oil phenolic compounds—hydroxytyrosol, tyrosol, oleuropein, oleocanthal and oleacein—the most important being their antiatherogenic, cardioprotective, anticancer, neuroprotective and endocrine effects. The evidence presented in the review concludes that these phenolic compounds have great pharmacological potential, however, further studies are still required.

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Section: Oleuropeinmentioning

confidence: 99%

Hydroxytyrosol, Tyrosol and Derivatives and Their Potential Effects on Human Health

et al. 2019

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“…Also, GSH critically functions in antioxidant defense and serves as a vital regulator of pathways essential for maintaining body homeostasis [ 43 ]. More importantly, decreased levels of TNF-α, IL-6, and MDA have been observed along with increased SOD and GSH levels have been previously documented following alleviation of MIRI after oleuropein treatment [ 44 ]. Collectively, these findings supported the inhibitory role of miR-206 overexpression in MIRI.…”

Section: Discussionmentioning

confidence: 98%

Histone deacetylase HDAC4 participates in the pathological process of myocardial ischemia-reperfusion injury via MEKK1/JNK pathway by binding to miR-206

Zhu

Niu

et al. 2021

Cell Death Discov.

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Histone deacetylases (HDACs) and microRNAs (miRs) have been reported to exert pivotal roles on the pathogenesis of myocardial ischemia-reperfusion injury (MIRI). Therefore, the present study was performed to define the underlying role of HDAC4 and miR-206 in the pathological process of MIRI. An IRI rat model was established. The interaction between HDAC4 and the promoter region of miR-206 was determined using ChIP, and that between miR-206 and mitogen-activated protein kinase kinase kinase 1 (MEKK1) was determined using dual luciferase reporter gene assay. After the loss- or gain-of-function assay in cardiomyocytes, western blot analysis, RT-qPCR, TUNEL, and ELISA assay were performed to define the roles of HDAC4, miR-206, and MEKK1. Up-regulation of HDAC4 and down-regulation of miR-206 occurred in rat myocardial tissues and cardiomyocytes in MIRI. HDAC4 down-regulation or miR-206 up-regulation contributed to reduced cell apoptosis and the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA), while elevating the superoxide dismutase (SOD) and glutathione (GSH) contents. Meanwhile, HDAC4 silencing promoted the expression of miR-206, which targeted and negatively regulated MEKK1. Then inhibition of JNK phosphorylation reduced the cardiomyocyte apoptosis to alleviate MIRI. Coherently, HDAC4 silencing could up-regulate the expression of miR-206 to reduce cardiomyocyte apoptosis and inhibit oxidative stress, and exerting a protective effect on MIRI via the MEKK1/JNK pathway.

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“…The mechanism of olea derivatives is still unknown. However, recent data showed that, in myocardial I/R rats, OL modulated the ERK pathway and suppressed the induction of p53, p-MEK, and p-ERK protein expression [ 60 ]. Cisplatin-induced acute renal injury was attenuated by OL through the inhibition of p53 and ERK signalling in mice [ 61 ].…”

Section: Candidates For Nutraceutical Supplementation In the Failimentioning

confidence: 99%

Pathophysiological Basis for Nutraceutical Supplementation in Heart Failure: A Comprehensive Review

et al. 2021

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There is evidence demonstrating that heart failure (HF) occurs in 1–2% of the global population and is often accompanied by comorbidities which contribute to increasing the prevalence of the disease, the rate of hospitalization and the mortality. Although recent advances in both pharmacological and non-pharmacological approaches have led to a significant improvement in clinical outcomes in patients affected by HF, residual unmet needs remain, mostly related to the occurrence of poorly defined strategies in the early stages of myocardial dysfunction. Nutritional support in patients developing HF and nutraceutical supplementation have recently been shown to possibly contribute to protection of the failing myocardium, although their place in the treatment of HF requires further assessment, in order to find better therapeutic solutions. In this context, the Optimal Nutraceutical Supplementation in Heart Failure (ONUS-HF) working group aimed to assess the optimal nutraceutical approach to HF in the early phases of the disease, in order to counteract selected pathways that are imbalanced in the failing myocardium. In particular, we reviewed several of the most relevant pathophysiological and molecular changes occurring during the early stages of myocardial dysfunction. These include mitochondrial and sarcoplasmic reticulum stress, insufficient nitric oxide (NO) release, impaired cardiac stem cell mobilization and an imbalanced regulation of metalloproteinases. Moreover, we reviewed the potential of the nutraceutical supplementation of several natural products, such as coenzyme Q10 (CoQ10), a grape seed extract, Olea Europea L.-related antioxidants, a sodium–glucose cotransporter (SGLT2) inhibitor-rich apple extract and a bergamot polyphenolic fraction, in addition to their support in cardiomyocyte protection, in HF. Such an approach should contribute to optimising the use of nutraceuticals in HF, and the effect needs to be confirmed by means of more targeted clinical trials exploring the efficacy and safety of these compounds.

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Inhibition of MEK/ERK/STAT3 signaling in oleuropein treatment inhibits myocardial ischemia/reperfusion

Cited by 17 publications

References 32 publications

Hydroxytyrosol, Tyrosol and Derivatives and Their Potential Effects on Human Health

Hydroxytyrosol, Tyrosol and Derivatives and Their Potential Effects on Human Health

Histone deacetylase HDAC4 participates in the pathological process of myocardial ischemia-reperfusion injury via MEKK1/JNK pathway by binding to miR-206

Pathophysiological Basis for Nutraceutical Supplementation in Heart Failure: A Comprehensive Review

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