Isoquercetin ameliorates myocardial infarction through anti-inflammation and anti-apoptosis factor and regulating TLR4-NF-κB signal pathway

Ma, Chengtai; Jiang, Yanxia; Zhang, Xiaohui; Chen, Xiaoxue; Liu, Zhenfang; Tian, Xintao

doi:10.3892/mmr.2018.8709

Cited by 23 publications

(23 citation statements)

References 31 publications

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“…Regarding in vivo effects of QCT derivatives in cardiac injury, it was documented that two weeks lasting treatment with isoQCT (80 mg/kg/day by gavage) protected male Sprague-Dawley rat hearts against acute myocardial infarction in vivo. IsoQCT protected myocardium through anti-inflammatory and anti-apoptotic effects, and via regulation of the TLR4-NF-κB signaling pathway [98]. Pretreatment of male Wistar rats with another QCT derivative troxerutin ((3 ,4 ,7-Tris[O-(2-hydroxyethyl)]rutin; 150 mg/kg for one month) protected myocardium against I/R injury (30 min/45 min) maintained by ligation of the left anterior descending artery.…”

Section: In Vivo Cardioprotection Afforded By Qct Derivativesmentioning

confidence: 99%

Potential Implications of Quercetin and its Derivatives in Cardioprotection

Ferenczyová

Kaločayová

Barteková

2020

IJMS

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Quercetin (QCT) is a natural polyphenolic compound enriched in human food, mainly in vegetables, fruits and berries. QCT and its main derivatives, such as rhamnetin, rutin, hyperoside, etc., have been documented to possess many beneficial effects in the human body including their positive effects in the cardiovascular system. However, clinical implications of QCT and its derivatives are still rare. In the current paper we provide a complex picture of the most recent knowledge on the effects of QCT and its derivatives in different types of cardiac injury, mainly in ischemia-reperfusion (I/R) injury of the heart, but also in other pathologies such as anthracycline-induced cardiotoxicity or oxidative stress-induced cardiac injury, documented in in vitro and ex vivo, as well as in in vivo experimental models of cardiac injury. Moreover, we focus on cardiac effects of QCT in presence of metabolic comorbidities in addition to cardiovascular disease (CVD). Finally, we provide a short summary of clinical studies focused on cardiac effects of QCT. In general, it seems that QCT and its metabolites exert strong cardioprotective effects in a wide range of experimental models of cardiac injury, likely via their antioxidant, anti-inflammatory and molecular pathways-modulating properties; however, ageing and presence of lifestyle-related comorbidities may confound their beneficial effects in heart disease. On the other hand, due to very limited number of clinical trials focused on cardiac effects of QCT and its derivatives, clinical data are inconclusive. Thus, additional well-designed human studies including a high enough number of patients testing different concentrations of QCT are needed to reveal real therapeutic potential of QCT in CVD. Finally, several negative or controversial effects of QCT in the heart have been reported, and this should be also taken into consideration in QCT-based approaches aimed to treat CVD in humans.

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Section: In Vivo Cardioprotection Afforded By Qct Derivativesmentioning

confidence: 99%

Potential Implications of Quercetin and its Derivatives in Cardioprotection

Ferenczyová

Kaločayová

Barteková

2020

IJMS

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“…On macroscopic examination, treatment with quercetin induced a significant reduction of myocardial infarct size on triphenyl tetrazolium chloride (TTC) staining (149)(150)(151). This was further supported by lower levels of serum creatine kinase (CK), CK-MB, cardiac troponin T and lactate dehydrogenase, all enzymatic markers of myocardial insult (144,(147)(148)(149)(151)(152)(153)(154)(155). Histopathological examinations also revealed lower infiltration of leukocytes to the site of infarction, less edema and overall maintained tissue architecture (149,152,153).…”

Section: Myocardial Protective Effects Of Quercetinmentioning

confidence: 88%

Therapeutic Potential of Quercetin to Alleviate Endothelial Dysfunction in Age-Related Cardiovascular Diseases

Dagher

Mury

Thorin‐Trescases

et al. 2021

Front. Cardiovasc. Med.

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The vascular endothelium occupies a catalog of functions that contribute to the homeostasis of the cardiovascular system. It is a physically active barrier between circulating blood and tissue, a regulator of the vascular tone, a biochemical processor and a modulator of coagulation, inflammation, and immunity. Given these essential roles, it comes to no surprise that endothelial dysfunction is prodromal to chronic age-related diseases of the heart and arteries, globally termed cardiovascular diseases (CVD). An example would be ischemic heart disease (IHD), which is the main cause of death from CVD. We have made phenomenal advances in treating CVD, but the aging endothelium, as it senesces, always seems to out-run the benefits of medical and surgical therapies. Remarkably, many epidemiological studies have detected a correlation between a flavonoid-rich diet and a lower incidence of mortality from CVD. Quercetin, a member of the flavonoid class, is a natural compound ubiquitously found in various food sources such as fruits, vegetables, seeds, nuts, and wine. It has been reported to have a wide range of health promoting effects and has gained significant attention over the years. A growing body of evidence suggests quercetin could lower the risk of IHD by mitigating endothelial dysfunction and its risk factors, such as hypertension, atherosclerosis, accumulation of senescent endothelial cells, and endothelial-mesenchymal transition (EndoMT). In this review, we will explore these pathophysiological cascades and their interrelation with endothelial dysfunction. We will then present the scientific evidence to quercetin's anti-atherosclerotic, anti-hypertensive, senolytic, and anti-EndoMT effects. Finally, we will discuss the prospect for its clinical use in alleviating myocardial ischemic injuries in IHD.

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“…The level of MDA, SOD, GPx, and MPO activities in myocardial tissues were quantified using commercial kits, according to the manufacturer’s instructions (Beyotime Institute of Biotechnology, Nanjing, China) 30…”

Section: Methodsmentioning

confidence: 99%

<p>Protective Effect Of Vasicine Against Myocardial Infarction In Rats Via Modulation Of Oxidative Stress, Inflammation, And The PI3K/Akt Pathway</p>

Jiang¹,

Zhang²,

Ding³

et al. 2019

DDDT

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BackgroundMyocardial infarction is the leading cause of damage to the heart and is classified as a major cause of death related to cardiovascular disease. In the present study, we intended to investigate the protective effect of vasicine (VAS) against myocardial infarction in rats, and its mechanism.MethodsMyocardial infarction was induced by isoproterenol (ISO, 100 mg/kg) at an interval of 24 h for 2 days. Different doses of VAS (2.5, 5, and 10 mg/kg body weight) were administered to the rats. The effect of VAS on oxidative stress markers such as, myocardial necrosis, myocardial ability and infarct volume, inflammatory cytokines, membrane-bound myocardial enzymes, and histopathological changes was investigated. Western blot analysis was also conducted to analyze the effect of VAS on autophagy (PI3K/Akt) and apoptosis (Bcl-2, Bax, and caspase-3). The number of apoptotic cells in the different groups was also identified using TUNEL.ResultsResults suggested that VAS causes reduction in myocardial necrosis by reduction of elevated LDH, CK-MB, and TnT levels. It also causes augmentation of left ventricular systolic pressure (LVSP) and myocardial contractility as determined in terms of +dp/dtmax and –dp/dtmax. Furthermore, VAS causes reduction of TNF-α and IL-6 levels. VAS also improved cardiac function via enhancing posterior wall thickness of the LV with concurrent increase in the mass of LV. In the present study, VAS caused activation of phosphorylated PI3K (p-PI3K) and phosphorylated Akt (p-Akt) in a dose-dependent manner. Furthermore, VAS suppressed apoptosis when tested on animals suffering from ISO-induced MI, by decreasing the expression of cleaved Caspase-3 and Bax while increasing the expression of Bcl-2.ConclusionIn conclusion, vasicine has a protective effect against MI in vivo, through inhibiting oxidative stress, inflammation and excessive autophagy, to suppress apoptosis via activation of the PI3K/Akt/mTOR signaling pathway.

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Isoquercetin ameliorates myocardial infarction through anti-inflammation and anti-apoptosis factor and regulating TLR4-NF-κB signal pathway

Cited by 23 publications

References 31 publications

Potential Implications of Quercetin and its Derivatives in Cardioprotection

Potential Implications of Quercetin and its Derivatives in Cardioprotection

Therapeutic Potential of Quercetin to Alleviate Endothelial Dysfunction in Age-Related Cardiovascular Diseases

<p>Protective Effect Of Vasicine Against Myocardial Infarction In Rats Via Modulation Of Oxidative Stress, Inflammation, And The PI3K/Akt Pathway</p>

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