Deodorized Garlic Decreases Oxidative Stress Caused by Lipopolysaccharide in Rat Heart through Hydrogen Sulfide: Preliminary Findings.
Israel Pérez-TorresLinaloe Manzano-PechVerónica Guarner-LansMaría Elena SotoVicente Castrejón-TéllezRicardo Márquez-VelascoÁlvaro Vargas-GonzálezRaúl Martínez-MemijeLeonardo Del Valle-MondragonJulieta Anabell Díaz-JuárezMaria Sanchez-AguilarJuan Carlos Torres-NarváezPublished in: International journal of molecular sciences (2022)
Deodorized garlic (DG) may favor the activity of the antioxidant enzymes and promote the synthesis of hydrogen sulfide (H 2 S). The objective was to test if DG favors an increase in H 2 S and if it decreases the oxidative stress caused by lipopolysaccharide (LPS) in rat hearts. A total of 24 rats were divided into 4 groups: Group 1 control (C), Group 2 LPS, Group 3 DG, and Group 4 LPS plus DG. The cardiac mechanical performance (CMP), coronary vascular resistance (CVR), and oxidative stress markers, such as total antioxidant capacity (TAC), glutathione (GSH), selenium (Se), lipid peroxidation (LPO), thiols, hydrogen sulfide (H 2 S), and the activities and expressions of thioredoxin reductase (TrxR), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), cystathionine synthetase (CBS), cystathionine γ-lyase (CTH), iNOS, and eNOS-p, were analyzed in the heart. Infarct zones in the cardiac tissue were present ( p = 0.01). The CMP and CVR decreased and increased ( p ≤ 0.05), TAC, GSH, H 2 S, NO, thiols, and GST activity ( p ≤ 0.01) decreased, and LPO and iNOS increased ( p ≤ 0.05). The activities and expressions of TrxR, GPx, eNOS- p , CTH, and CBS ( p ≤ 0.05) decreased with the LPS treatment; however, DG normalized this effect. DG treatment decreases heart damage caused by LPS through the cross-talk between the H 2 S and NO systems.
Keyphrases
- oxidative stress
- inflammatory response
- anti inflammatory
- dna damage
- diabetic rats
- heart failure
- nitric oxide synthase
- ischemia reperfusion injury
- lps induced
- induced apoptosis
- toll like receptor
- left ventricular
- atrial fibrillation
- coronary artery
- coronary artery disease
- endothelial cells
- acute myocardial infarction
- heat shock
- signaling pathway
- endoplasmic reticulum stress
- replacement therapy
- acute coronary syndrome
- aortic stenosis
- ejection fraction