The impacts of vorinostat on NADPH oxidase and mitochondrial biogenesis gene expression in the heart of mice model of depression

The comorbidity of depression and high risk of cardiovascular diseases (CVD) have been reported as major health problems. Our previous study confirmed that fluoxetine (FLX) therapy had a significant influence on brain function but not on the heart in depression. In the present study, suberoyanilide...

Full description

Saved in:
Bibliographic Details
Published in:Canadian journal of physiology and pharmacology 2022-11, Vol.100 (11), p.1077-1085
Main Authors: Nasehi, Leila, Morassaei, Bahareh, Ghaffari, Maryam, Sharafi, Ali, Dehpour, Ahmad Reza, Hosseini, Mir-Jamal
Format: Article
Language:English
Subjects:
Biosynthesis
Cardiovascular diseases
Comorbidity
Complications and side effects
Depression, Mental
Development and progression
Dosage and administration
Drug therapy
Fluoxetine
GA-binding protein
Gene expression
Health aspects
Heart
Hydroxamic acid
Mental depression
Mitochondria
NAD(P)H oxidase
NADP (Coenzyme)
Oxidases
Patients
Peroxisome proliferator-activated receptors
Physiological aspects
Risk factors
Vorinostat
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The comorbidity of depression and high risk of cardiovascular diseases (CVD) have been reported as major health problems. Our previous study confirmed that fluoxetine (FLX) therapy had a significant influence on brain function but not on the heart in depression. In the present study, suberoyanilide hydroxamic acid (SAHA) was proposed as another therapeutic candidate for treatment of depression comorbid CVD in maternal separation model, following behavioral analyses and gene expression level in the heart. Our data demonstrated that SAHA significantly attenuates the gene expression level in treated mice with SAHA and FLX without significant change in expression level. SAHA decreased the gene expression level of peroxisome proliferator-activated receptor-gamma coactivator ) and nuclear respiratory factors (Nrf2) in heart tissues of maternally separated mice. It supposed that non-effectiveness of FLX on mitochondrial biogenesis and NOX gene expression level in the heart of depressed patient can be related to recurrence of depression. It revealed that SAHA not only reversed the depressive-like behavior similar to our previous data but also recovered the heart mitochondrial function via effect on , and mitochondrial biogenesis genes' (PGC-1 , Nrf-2, and peroxisome proliferator-activated receptor- (PPAR- ) expression levels. We suggest performing more studies to confirm SAHA as a therapeutic candidate in depression comorbid CVD.
ISSN:0008-4212
1205-7541
DOI:10.1139/cjpp-2022-0098