Hesperidin Attenuates Oxidative Stress, Inflammation, Apoptosis, and Cardiac Dysfunction in Sodium Fluoride-Induced Cardiotoxicity in Rats.
Behçet VarışlıEkrem DarendelioğluCüneyt ÇaglayanFatih Mehmet KandemirAdnan AynaAydın GençÖzge KandemirPublished in: Cardiovascular toxicology (2022)
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.
Keyphrases
- oxidative stress
- diabetic rats
- cell death
- signaling pathway
- anti inflammatory
- heat shock protein
- induced apoptosis
- heat shock
- pet ct
- gene expression
- heat stress
- high glucose
- heart failure
- left ventricular
- dna damage
- pi k akt
- rheumatoid arthritis
- poor prognosis
- simultaneous determination
- drinking water
- epithelial mesenchymal transition
- genome wide
- ischemia reperfusion injury
- mass spectrometry
- drug induced
- physical activity
- atrial fibrillation
- body mass index
- dna methylation
- combination therapy
- immune response
- fatty acid
- inflammatory response
- multiple sclerosis
- solid phase extraction
- cerebral ischemia
- resting state
- single molecule
- nuclear factor
- protein kinase
- high resolution mass spectrometry
- single cell
- weight loss
- brain injury