Melatonin protects H9c2 cells against ischemia/reperfusion‑induced apoptosis and oxidative stress via activation of the Nrf2 signaling pathway

Zhang, Yan; Qiao, Baoguang; Gao, Fei; Wang, Haifeng; Miao, Shaohua; Zhao, Huan

doi:10.3892/mmr.2018.9315

Cited by 17 publications

(15 citation statements)

References 36 publications

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“…A recent study by Zhang et al has shown the protective effects of melatonin on H9C2 cells 56 . They acknowledged that melatonin could reduce oxidative stress and IR‐induced cellular apoptosis by activating the Nrf2 signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

An innovative approach to fabricate a thermosensitive melatonin‐loaded conductive pluronic/chitosan hydrogel for myocardial tissue engineering

Torabi

Mehdikhani

Varshosaz

et al. 2020

J of Applied Polymer Sci

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This study aimed at designing and fabrication of a novel injectable and thermosensitive melatonin‐loaded pluronic/chitosan hydrogel containing gold nanoparticles (GNPs) and poly glycerol sebacate (PGS) for myocardial tissue engineering. The PGS nanoparticles were used as the melatonin (drug model) carrier. The gelation time, syringeability, stability, and swelling of the hydrogel were scrutinized. Rheological properties, chemical composition, and morphology of the samples were also investigated. The effect of GNPs addition on the electrical conductivity of hydrogel was assessed. The cytotoxicity of hydrogels was assessed through MTT assay in the exposure of H9C2 cells up to 7 days. Scanning electron microscopy was applied to evaluate the morphology of seeded cells. The synthesis parameters of PGS nanoparticles were optimized through which 2.5%w/v of PGS and 1:10 organic phase to aqueous phase (O/A) ratio were found desirable. The optimum hydrogel illustrated 2 min gelation time and was stable up to 20 days with 5% swelling in the first 12 h into phosphate buffered saline. The GNPs with a uniform distribution rendered the hydrogel electrically conductive (1500 μS/cm). According to the MTT assay results, 3.125 μM melatonin was considered as the suitable concentration by which a significant increase in the cell viability was observed. The results exhibited that the prepared hydrogel composed of pluronic/chitosan/GNPs, and 3.125 μM melatonin‐loaded PGS nanoparticles could be applied as a promising scaffold for myocardial tissue engineering.

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Section: Resultsmentioning

confidence: 99%

An innovative approach to fabricate a thermosensitive melatonin‐loaded conductive pluronic/chitosan hydrogel for myocardial tissue engineering

Torabi

Mehdikhani

Varshosaz

et al. 2020

J of Applied Polymer Sci

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“…Zhang et al [ 84 ] suggested that melatonin may protect H9c2 cells against IRI by reducing apoptosis and oxidative stress, mediated via activation of the Nrf2 signaling pathway. The protective effect of atorvastatin is generated via the inhibition of neutrophil infiltration, TNF-α production, and activation of the Nrf2/ARE pathway, leading to upregulation of HO-1, a sensitive and reliable indicator of cellular oxidative stress [ 85 ].…”

Section: Nrf2/keap1/are Pathway As a Potential Target In Iri Therapymentioning

confidence: 99%

Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

Uçar

Saha³

et al. 2021

Antioxidants

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Ischemia/reperfusion (I/R) injury is associated with substantial clinical implications, including a wide range of organs such as the brain, kidneys, lungs, heart, and many others. I/R injury (IRI) occurs due to the tissue injury following the reestablishment of blood supply to ischemic tissues, leading to enhanced aseptic inflammation and stimulation of oxidative stress via reactive oxygen and nitrogen species (ROS/RNS). Since ROS causes membrane lipids’ peroxidation, triggers loss of membrane integrity, denaturation of proteins, DNA damage, and cell death, oxidative stress plays a critical part in I/R pathogenesis. Therefore, ROS regulation could be a promising therapeutic strategy for IRI. In this context, Nrf2 (NF-E2-related factor 2) is a transcription factor that regulates the expression of several factors involved in the cellular defense against oxidative stress and inflammation, including heme oxygenase-1 (HO-1). Numerous studies have shown the potential role of the Nrf2/HO-1 pathway in IRI; thus, we will review the molecular aspects of Nrf2/Kelch-like ECH-associated protein 1 (Keap1)/antioxidant response element (ARE) signaling pathway in I/R, and we will also highlight the recent insights into targeting this pathway as a promising therapeutic strategy for preventing IRI.

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“…7 Supported by another study, the positive role of NRF2 in MI/RI has been confirmed that activation of NRF2 signaling pathway prevents I/Rinduced oxidative stress and apoptosis. 29 Additionally, an activator of NRF2, sulforaphane is reported to preserve cardiac function, reduce IS, oxidative stress and inflammation in MI/RI. 30 In contrast, downregulation of NRF2 is powerful to generate ROS and exacerbate OGD/R-induced injury in MI/RI.…”

Section: Nrf2 and Mir-29a-3p Are Downregulated While Ccnt2 Is Up-regulated In Cardiomyocytes In H/r Injury And Mir-29a-3p Targets Ccnt2mentioning

confidence: 99%

Restoration of NRF2 attenuates myocardial ischemia reperfusion injury through mediating microRNA‐29a‐3p/CCNT2 axis

et al. 2021

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Accumulated studies have been implemented for comprehending the mechanism of myocardial ischemia reperfusion injury (MI/RI). Nuclear factor erythroid-2 related factor 2 (NRF2)-mediated transcription activity in MI/RI has not been completely interpreted from the perspective of microRNA-29a-3p (miR-29a-3p) and cyclin T2 (CCNT2). Therein, this study intends to decode the mechanism of NRF2/miR-29a-3p/CCNT2 axis in MI/RI. Rat MI/RI models were established by left anterior descending artery ligation. Rats were injected with NRF2 or CCNT2 overexpression plasmids or miR-29a-3p agomir to explore their effects on MI/RI. Hypoxia/reoxygenation (H/R) cardiomyocytes were established and transfected with restored NRF2 or miR-29a-3p or CCNT2 for further exploration of their roles. NRF2, miR-29a-3p, and CCNT2 expression in myocardial tissues in rats with MI/RI and in cardiomyocytes in H/R injury were detected. ChIP assay verified the relationship between miR-29a-3p and NRF2, and the bioinformatics software and dual-luciferase reporter experiment verified the interaction between miR-29a-3p and CCNT2. NRF2 and miR-29a-3p were down-regulated while CCNT2 was up-regulated in myocardial tissues in rats with MI/RI and in H/R-treated cardiomyocytes. Restoration of NRF2 or miR-29a-3p improved hemodynamics and myocardial injury and

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Melatonin protects H9c2 cells against ischemia/reperfusion‑induced apoptosis and oxidative stress via activation of the Nrf2 signaling pathway

Cited by 17 publications

References 36 publications

An innovative approach to fabricate a thermosensitive melatonin‐loaded conductive pluronic/chitosan hydrogel for myocardial tissue engineering

An innovative approach to fabricate a thermosensitive melatonin‐loaded conductive pluronic/chitosan hydrogel for myocardial tissue engineering

Pharmacological Protection against Ischemia-Reperfusion Injury by Regulating the Nrf2-Keap1-ARE Signaling Pathway

Restoration of NRF2 attenuates myocardial ischemia reperfusion injury through mediating microRNA‐29a‐3p/CCNT2 axis

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