Troxerutin Preconditioning and Ischemic Postconditioning Modulate Inflammatory Response after Myocardial Ischemia/Reperfusion Injury in Rat Model

Badalzadeh, Reza; Baradaran, Behzad; Alihemmati, Alireza; Yousefi, Bahman; Abbaszadeh, A.

doi:10.1007/s10753-016-0462-8

Cited by 33 publications

(30 citation statements)

References 31 publications

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“…Rats treated with troxerutin exhibited significantly reduced myocardial infarct size, improved cardiac function likely via the modulated PI3K/Akt pathway [99]. Concordantly, treatment of male Wistar rats with troxerutin (150 mg/kg daily for one month) protected isolated hearts against I/R (30 min/45 min) injury via the inhibition of myocardial inflammatory cytokines TNF-α and IL-1β and inhibited activation of leukocyte-endothelial cell interaction molecule (ICAM-1) after I/R insult [100]. Plants such as stonebreaker (Phyllanthus amarus) and bitter gourd (Momordica charantia) represent good sources of antioxidants and QCT, as well as its derivatives quercitrin, isoquercitrin and rutin.…”

Section: In Vivo Cardioprotection Afforded By Qct Derivativesmentioning

confidence: 83%

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: 83%

Potential Implications of Quercetin and its Derivatives in Cardioprotection

Ferenczyová

Kaločayová

Barteková

2020

IJMS

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“…On the other hand, blocking the Ca 2+ channel has been shown to be effective in preventing reperfusion arrhythmias in rats. In a study by Farkas et al it was reported that the administration of verapamil and mibferadial before the main ischemia have elicited anti-arrhythmic effects in isolated rat hearts (26). Other studies have revealed that anti-arrhythmic influence of Ca 2+ antagonists is attributable to the inhibition of slow inward ionic current (27,28); the site of action of these agents is likely the ischemic zone.…”

Section: Discussionmentioning

confidence: 99%

The effects of mebudipine on myocardial arrhythmia induced by ischemia-reperfusion injury in isolated rat heart

Ghiasi

Mohammadi

Majidinia

et al. 2016

Cell Mol Biol (Noisy-le-grand)

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Reperfusion of the heart after an ischemic insult may lead to potentially lethal arrhythmias and cardimyocyte cell death via apoptosis and necrosis. In addition, previous studies showed that calcium channel blockers may have a protective role in the myocardium against arrhythmia and irreversible tissue injury. Therefore, this study was aimed to investigate the effects of mebudipine on myocardial arrhythmias and tissue injury induced by ischemia/reperfusion injury in isolated rat hearts. Male Wistar rats (250‑300g) were randomly divided to Sham group (without ischemia), control group (ischemia without drug), drug group (ischemia with mebudipine 0.1nM) and vehicle group (ischemia with ethanol 0.01%). The hearts of anaesthetized rats were removed and mounted on Langendorff apparatus and perfused by Krebs‑Henseleit solution under constant pressure of 75 mmHg at 37°C. Impulsive heart rate was monitored with bipolar golden electrodes. The electrocardiographs were recorded throughout the experiment and interpreted using the Lambeth convention. LDH and CPK activities in coronary effluent were analyzed spectrophotometrically. Hematoxilin & Eosin staining was performed for evaluation of microscopic architecture of the myocardium and tissue injury. Pretreatment with mebudipine significantly decreased the number of ventricular premature beats (VPB) as compared with control group. The similar findings were seen in the number of ventricular tachycardia (VT) and fibrillation (VF) among groups. In addition, mebudipine significantly reduced the severity of arrhythmias in comparison with control hearts. Moreover, the drug group demonstrated marked improvement in edema and infiltration of inflammatory cells especially with regard to the degree of myonecrosis and cell lysis.Mebudipine diminished the number and the incidence of myocardial arrhythmias induced by reperfusion injury and the severity of tissue injury.

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“…C). In addition, the elevation of cTn1 and CK‐MB expression are well‐known used as cardiac biomarkers .…”

Section: Resultsmentioning

confidence: 99%

Cilostazol protects against myocardial ischemia and reperfusion injury by activating transcription factor EB (TFEB)

Xiang

2019

Biotech and App Biochem

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Although cilostazol was proved to have antitumor biological effects, its function in myocardial ischemia and reperfusion (I/R) injury and the underlying mechanisms were not fully illustrated yet. In this study, a rat model of I/R injury was constructed and quantitative real-time PCR, Western blot, and immunofluorescence (IF) assay were performed. Our results showed that cilostazol increased LC3 II/LC3 I ratio, reduced p62 abundance, and promoted the expressions of LAMP1, LAMP2, cathepsin B, and cathepsin D, indicating that cilostazol could activate autophagy and elevated lysosome activation. Following analysis showed that cilostazol enhanced nuclear protein expression of transcription factor EB (TFEB), an important regulator of autophagy-lysosome pathway. Furthermore, CCI-779, an inhibitor of TFEB, could reverse the effects of cilostazol on autophagic activity and lysosome activation. Importantly, cilostazol suppressed I/R injury-induced apoptosis by decreasing the cleavage of caspase 3 and PARP. Enzyme-linked immunosorbent assay showed that cilostazol reduced the serum levels of CTn1 and CK-MB and decreased infract size caused by I/R injuries. Altogether this study suggested that cilostazol protects against I/R injury by regulating autophagy, lysosome, and apoptosis in a rat model of I/R injury. The protective mechanism of cilostazol was partially through increasing the transcriptional activity of TFEB.

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Troxerutin Preconditioning and Ischemic Postconditioning Modulate Inflammatory Response after Myocardial Ischemia/Reperfusion Injury in Rat Model

Cited by 33 publications

References 31 publications

Potential Implications of Quercetin and its Derivatives in Cardioprotection

Potential Implications of Quercetin and its Derivatives in Cardioprotection

The effects of mebudipine on myocardial arrhythmia induced by ischemia-reperfusion injury in isolated rat heart

Cilostazol protects against myocardial ischemia and reperfusion injury by activating transcription factor EB (TFEB)

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