Lutein exerts its cardioprotective effect against the experimental model of isoprenaline‐induced myocardial infarction via MIAT/miR‐200a/Nrf2/TXINP pathway

Abdelmonem, Maha; Ibrahim, Sherehan M.; Essam, Reham M.; Amin, Hebat Allah; Abd-Elmawla, Mai A.

doi:10.1002/jbt.22899

Cited by 16 publications

(6 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The nuclear factor erythroid 2-related factor 2 (Nrf2) is a nuclear transcription factor that regulates redox status of the cells via modulating antioxidant systems, with simultaneous antiinflammatory activity. [9,10] Nrf2 binds to antioxidant response elements in the promoter region of genes encoding many antioxidants and detoxifying enzymes. [11] Glutathione (GSH) can act as a scavenger for ROS and as a cofactor for certain detoxifying enzymes that reduces, and thus, regenerates antioxidants.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol mitigates diclofenac‐induced hepatorenal toxicity in rats via modulation of miR‐144/Nrf2/GSH axis

Elbaz

Ahmed

Abdelmonem

2022

J Biochem & Molecular Tox

Self Cite

View full text Add to dashboard Cite

Despite the extensive therapeutic uses of diclofenac, it may cause several adverse effects, including hepatorenal injury. The antioxidant and anti-inflammatory properties of resveratrol, a polyphenolic compound, make the agent effective in ameliorating a variety of drug-induced injuries. This study investigated the potential beneficial effects of resveratrol on diclofenac-induced hepatorenal toxicity and explored the role of miR-144 and its relationship to oxidative stress and inflammation triggered by diclofenac. Rats were divided into four groups: control; diclofenac group received diclofenac (10 mg/kg/day, intraperitoneal [ip]) for 7 days; prevention group received resveratrol concomitantly with diclofenac for 7 days; and the treatment group received diclofenac for 7 days followed by resveratrol (20 mg/kg/day, per oral) for another 7 days. Diclofenac administration induced a significant increase in serum hepatorenal biomarkers and histopathological aberrations. In addition, diclofenac upregulated miR-144 while reducing nuclear factor erythroid 2-related factor 2 (Nrf2) protein levels and glutathione (GSH) content.Moreover, diclofenac induced tissue inflammation and apoptosis as evidenced by increased protein expression of nuclear factor kappa B (NF-κB), tumor necrosis factor α (TNF-α), and caspase-3. Intriguingly, resveratrol prevention or treatment significantly mitigated the toxic effects of diclofenac as manifested by normalization of the hepatorenal functions and amelioration of the histopathological changes.Resveratrol also triggered miR-144 downregulation with Nrf2 upregulation.Consequently, resveratrol showed hepatorenal antioxidant, anti-inflammatory, and antiapoptotic activities as manifested by improvement in the antioxidant markers along with a decline in NF-κB, TNF-α, and caspase-3 expressions. In conclusion, this study demonstrates a potential therapeutic role of resveratrol in mitigating diclofenac-induced hepatorenal insult, possibly via modulating miR-144/Nrf2/ GSH axis.

show abstract

Section: Introductionmentioning

confidence: 99%

Resveratrol mitigates diclofenac‐induced hepatorenal toxicity in rats via modulation of miR‐144/Nrf2/GSH axis

Elbaz

Ahmed

Abdelmonem

2022

J Biochem & Molecular Tox

Self Cite

View full text Add to dashboard Cite

show abstract

“… 28 Homo sapiens was selected for analysis, and the standard names of all protein targets were matched through UniProt ( https://www.uniprot.org/ ). 29 Component and disease targets were searched for intersections and introduced into Cytoscape 3.7.2 to construct network maps. Then, the intersecting targets were imported into String ( https://string-db.org/ ) to build a PPI network.…”

Section: Methodsmentioning

confidence: 99%

Network Pharmacology-Based Combined with Experimental Validation Study to Explore the Underlying Mechanism of Agrimonia pilosa Ledeb. Extract in Treating Acute Myocardial Infarction

Chen¹,

Wang²,

Kang³

et al. 2022

DDDT

View full text Add to dashboard Cite

Purpose The network pharmacology approach and validation experiment were performed to investigate the potential mechanisms of Agrimonia pilosa Ledeb . (APL) extract against acute myocardial infarction (AMI). Methods The primary compounds of APL extract were identified by High-Performance Liquid Chromatography (HPLC) analysis. The intersecting targets of active compounds and AMI were determined via network pharmacology analysis. A mouse model of AMI was established by subcutaneous injection of isoproterenol (Iso). Mice were treated with APL extract by intragastric administration. We assessed the effects of APL extract on the electrocardiography (ECG), cardiac representative markers, representative indicators of oxidative stress, pathological changes, and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, as well as apoptosis-related indicators in the mice. Results Five candidate compounds were identified in APL extract. Enrichment analyses indicated that APL extract could exert myocardial protective effects via the PI3K/Akt pathway. ST segment elevation and increased heart rate were obviously reversed in APL extract groups compared to Iso group. We also detected significant decreases in lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase MB (CK-MB), malondialdehyde (MDA), and reactive oxygen species (ROS), as well as a significant increase in superoxide dismutase activities (SOD) after APL extract treatment. In addition, APL extract markedly decreased the number of apoptotic cardiomyocytes after AMI. In the APL extract groups of AMI mice, there were increased expression levels of p-PI3K, p-Akt, and B-cell lymphoma-2 (Bcl-2) protein, and there were decreases in Bcl-2-associated X (Bax), cysteinyl aspartate-specific proteases-3 (caspase-3), and cleaved-caspase-3 protein expression levels, as well as the Bax/Bcl-2 ratio. Conclusion APL extract had a protective effect against Iso-induced AMI. APL extract could ameliorate AMI through antioxidant and anti-apoptosis actions which may be associated with the activation of the PI3K/Akt signaling pathway.

show abstract

“…Furthermore, lutein possesses a cardio-protective role in AMI by downregulating MIAT (Abdelmonem et al, 2021). Although these reports have uncovered the causal role and partial mechanism of MIAT in the pathogenesis of AMI, our understanding of its molecular determinants is still limited.…”

Section: Introductionmentioning

confidence: 99%

“…Under hypoxic conditions, MIAT could repress transcription via binding to SF1 and then induce cardiomyocyte pyroptosis (Zhou, 2022), and its knockdown might relieve cardiac function damage in MI mice through microRNA (miR)‐10a‐5p/EGR2 axis (Cao et al, 2021). Furthermore, lutein possesses a cardio‐protective role in AMI by downregulating MIAT (Abdelmonem et al, 2021). Although these reports have uncovered the causal role and partial mechanism of MIAT in the pathogenesis of AMI, our understanding of its molecular determinants is still limited.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of long noncoding RNA MIAT attenuates hypoxia‐induced cardiomyocyte injury by regulating the miR‐488‐3p/Wnt/β‐catenin pathway

Zhang

et al. 2022

Cell Biology International

View full text Add to dashboard Cite

Dysfunction of cardiomyocytes contributes to the development of acute myocardial infarction (AMI). Nonetheless, the regulatory mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in cardiomyocyte injury remains largely unclear. The cardiomyocyte injury was assessed via cell viability and apoptosis using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) and flow cytometry, respectively. The levels of MIAT, microRNA (miR)-488-3p, and Wnt5a were detected via quantitative real-time polymerase chain reaction and Western blot.After bioinformatical analysis, the binding between miR-488-3p and MIAT or Wnt5a was confirmed via dual-luciferase reporter, RNA immunoprecipitation, and RNA pulldown assays. Our results showed that MIAT expression was increased in AC16 cells after hypoxia treatment. Silencing of MIAT alleviated hypoxia-induced viability reduction, apoptosis increase, and Wnt/β-catenin pathway activation. MIAT directly targeted miR-488-3p. MiR-488-3p might repress hypoxia-induced cardiomyocyte injury, and its knockdown reversed the effect of MIAT depletion on cardiomyocyte injury. Wnt5a was validated as a target of miR-488-3p. Wnt5a expression restoration attenuated the influence of MIAT knockdown on hypoxia-triggered cardiomyocyte injury. Our findings demonstrated that downregulation of MIAT might mitigate hypoxia-induced cardiomyocyte injury partly through miR-488-3p mediated Wnt/β-catenin pathway.

show abstract

Lutein exerts its cardioprotective effect against the experimental model of isoprenaline‐induced myocardial infarction via MIAT/miR‐200a/Nrf2/TXINP pathway

Cited by 16 publications

References 44 publications

Resveratrol mitigates diclofenac‐induced hepatorenal toxicity in rats via modulation of miR‐144/Nrf2/GSH axis

Resveratrol mitigates diclofenac‐induced hepatorenal toxicity in rats via modulation of miR‐144/Nrf2/GSH axis

Network Pharmacology-Based Combined with Experimental Validation Study to Explore the Underlying Mechanism of Agrimonia pilosa Ledeb. Extract in Treating Acute Myocardial Infarction

Knockdown of long noncoding RNA MIAT attenuates hypoxia‐induced cardiomyocyte injury by regulating the miR‐488‐3p/Wnt/β‐catenin pathway

Contact Info

Product

Resources

About