Evidence map›Paper›PMID 38796673›Full record

ArticleMolecular biology reports2024

Chrysin reduces heart endoplasmic reticulum stress-induced apoptosis by inhibiting PERK and Caspase 3-7 in high-fat diet-fed rats.

Subramani Yuvaraj, Varadaraj Vasudevan, Shanavas Syed Mohamed Puhari, Sunderasan Sasikumar, Tharmarajan Ramprasath, Mariaraj Sivakumar Selvi, Govindan Sadasivam Selvam

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

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5citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Subramani YuvarajMolecular Cardiology Unit, Department of Biochemistry, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai, Tamil Nadu, 625021, India.
Varadaraj VasudevanMolecular Cardiology Unit, Department of Biochemistry, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai, Tamil Nadu, 625021, India.
Shanavas Syed Mohamed PuhariMolecular Cardiology Unit, Department of Biochemistry, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai, Tamil Nadu, 625021, India.
Sunderasan SasikumarMolecular Cardiology Unit, Department of Biochemistry, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai, Tamil Nadu, 625021, India.
Tharmarajan RamprasathCenter for Molecular and Translational Medicine, Georgia State University, Atlanta, GA, USA.
Mariaraj Sivakumar SelviMolecular Cardiology Unit, Department of Biochemistry, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai, Tamil Nadu, 625021, India.
Govindan Sadasivam SelvamMolecular Cardiology Unit, Department of Biochemistry, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai, Tamil Nadu, 625021, India. drselvamgsbiochem@rediffmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChrysin (Chy) is a naturally occurring flavonoid found in fruits, vegetables, honey, propolis, and many plant extracts that has shown notable medicinal value. Chy exhibits diverse pharmacological properties, including anti-oxidative, anti-inflammatory, anti-apoptotic, anti-cholesteremic, and cardioprotective. However, the influence of Chy in mitigating high-fat diet (HFD)-induced ER stress of rat myocardium remains unknown. PURPOSE: The current work intended to determine the therapeutic potential of Chy against HFD-induced endoplasmic stress-mediated apoptosis.

methodsTo evaluate the therapeutic value of Chy in HFD-induced endoplasmic stress-mediated apoptosis in the myocardium; The male wistar rats were divided into different groups; control, HFD control, HFD fed followed by Chy-treated and HFD fed followed by atorvastatin (Atv) treated rats.

resultsWhen compared to the control group, the HFD-fed rats had significantly higher levels of marker enzymes such as CK-NAC and ALP, as well as lipid peroxidation and lipid profile (TC, TG, LDL, and VLDL). Chy therapy greatly reversed these marker enzymes and the lipid profile. qRT-PCR Studies showed that Chy supplementation considerably improved Nrf2 and its target genes. In addition, Chy lowered the expression of PERK, CHOP, ATF6, GRP78, and Caspase-3 genes in the heart tissue of HFD-fed rats. Immunohistochemistry results demonstrated that Chy substantially enhanced the Nrf2 and reduced PERK and Caspase3-7 protein expression in HFD-fed rats.

conclusionThe current study concluded that Chy may mediate the cardioprotective effect by activating Nrf2 and inhibiting PERK signaling pathway against ER stress-mediated apoptosis induced by HFD. Therefore, supplementation with Chy could serve as a promising therapeutic target against HFD-induced ER stress-mediated cardiac complication.

Indexed as

ApoptosisDiet, High-FateIF-2 KinaseEndoplasmic Reticulum StressFlavonoidsMyocardiumRats, WistarAnimalsCaspase 3MaleNF-E2-Related Factor 2RatsSignal TransductionCaspase 3chrysineIF-2 KinaseFlavonoidsNF-E2-Related Factor 2ApoptosisAtherosclerosisChrysinEndoplasmic reticulum stressHypercholesterolemiaOxidative stress

Identifiers

PMID38796673

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.