ArticleCardiovascular toxicology2022
Hesperidin Attenuates Oxidative Stress, Inflammation, Apoptosis, and Cardiac Dysfunction in Sodium Fluoride-Induced Cardiotoxicity in Rats.
Article in Cardiovascular toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 41 citations in OpenAlex.
- Hesperidin Attenuates Mercury Chloride-Induced Neurotoxicity in Rats by Modulating Oxidative Stress, Neuroinflammation, Apoptosis, Autophagy and ER Stress.Biological trace element research · 2026Article
- Hesperidin: A Multifunctional Flavonoid with Therapeutic Potential in the Management of Pathogenesis.International journal of molecular sciences · 2026Review
- Protective Role of Hesperidin Against Deltamethrin-Induced Cardiovascular Structural Damage: Involvement of Caspase-3-Driven Apoptosis and Fibrosis Suppression in Rats.Journal of cardiovascular development and disease · 2026Article
- The Protective Effects of Chrysin on Acrylamide-Induced Hepatotoxicity: Insights Into Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Histological Evaluation in Rats.Journal of biochemical and molecular toxicology · 2025Article
- Plant Polyphenols as Heart's Best Friends: From Health Properties, to Cellular Effects, to Molecular Mechanisms of Action.International journal of molecular sciences · 2025Review
- Hesperidin alleviates hypothyroidism-related cardiac dysfunction by targeting cardiac miRNAs, Nrf2/NF-κB signaling, oxidative stress and inflammation.Frontiers in pharmacology · 2025Article
- Review
- Smart Hesperidin/Chitosan Nanogel Mitigates Apoptosis and Endoplasmic Reticulum Stress in Fluoride and Aluminum-Induced Testicular Injury.Biological trace element research · 2024Article
- In vitro evaluation of PLGA loaded hesperidin on colorectal cancer cell lines: an insight into nano delivery system.BMC biotechnology · 2024Article
- Hesperidin ameliorates HJournal of animal science and biotechnology · 2024Article
- Hesperidin counteracts chlorpyrifos-induced neurotoxicity by regulating oxidative stress, inflammation, and apoptosis in rats.Metabolic brain disease · 2024Article
- Cyclosporine-induced kidney damage was halted by sitagliptin and hesperidin via increasing Nrf2 and suppressing TNF-α, NF-κB, and Bax.Scientific reports · 2024Article
- Fermented Rooibos tea (Aspalathus linearis) Ameliorates Sodium Fluoride-Induced Cardiorenal Toxicity, Oxidative Stress, and Inflammation via Modulation of NF-κB/IκB/IκKB Signaling Pathway in Wistar Rats.Cardiovascular toxicology · 2024Article
- Histone methyltransferase SUV39H2 regulates apoptosis and chemosensitivity in prostate cancer through AKT/FOXO signaling pathway.Medical oncology (Northwood, London, England) · 2024Article
- Effects of chrysin in cadmium-induced testicular toxicity in the rat; role of multi-pathway regulation.Molecular biology reports · 2023Article
- Lemon-derived nanovesicles achieve antioxidant and anti-inflammatory effects activating the AhR/Nrf2 signaling pathway.iScience · 2023Article
- Xanthomicrol: Effective therapy for cancer treatment.Toxicology reports · 2023Review
- Cellular Antioxidant Properties ofMolecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive fluoride intake has been reported to cause toxicities to brain, thyroid, kidney, liver and testis tissues. Hesperidin (HSP) is an antioxidant that possesses anti-allergenic, anti-carcinogenic, anti-oxidant and anti-inflammatory activities. Presently, the studies focusing on the toxic effects of sodium fluoride (NaF) on heart tissue at biochemical and molecular level are limited. This study was designed to evaluate the ameliorative effects of HSP on toxicity of NaF on the heart of rats in vivo by observing the alterations in oxidative injury markers (MDA, SOD, CAT, GPX and GSH), pro-inflammatory markers (NF-κB, IL-1β, TNF-α), expressions of apoptotic genes (caspase-3, -6, -9, Bax, Bcl-2, p53, cytochrome c), levels of autophagic markers (Beclin 1, LC3A, LC3B), expression levels of PI3K/Akt/mTOR and cardiac markers. HSP treatment attenuated the NaF-induced heart tissue injury by increasing activities of SOD, CAT and GPx and levels of GSH, and suppressing lipid peroxidation. In addition, HSP reversed the changes in expression of apoptotic (caspase-3, -6, -9, Bax, Bcl-2, p53, cytochrome c), levels of autophagic and inflammatory parameters (Beclin 1, LC3A, LC3B, NF-κB, IL-1β, TNF-α), in the NaF-induced cardiotoxicity. HSP also modulated the gene expression levels of PI3K/Akt/mTOR signaling pathway and levels of cardiac markers (LDH, CK-MB). Overall, these findings reveal that HSP treatment can be used for the treatment of NaF-induced cardiotoxicity.
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Registered trials
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.