Quercetin modulates age-induced changes in the transcript levels of some apoptosis related genes in the skeletal muscles of male rats

• Published in: Brazilian Journal of Pharmaceutical Sciences Vol. 56
• Main Authors: Alm-Eldeen, Abeer, Khamis, Abeer, Elfiky, Nabil, Ahmad, Randa
• Format: Journal Article
• Language: English; Portuguese
• Published: Sao Paulo Universidade de Sao Paulo Faculdade de Ciencias 01.01.2020; Universidade de São Paulo, Faculdade de Ciências Farmacêuticas; Universidade de São Paulo
• Subjects: Age; Age, Bcl2; Aging; Antioxidants; Apoptosis; Bax; Caspace3; Catalase; Enzymes; Gene expression; Histopathology; MDA; NF-KB; Oxidative stress; PHARMACOLOGY & PHARMACY; Quercetin; Sarcopenia; Statistical analysis; Histopathology; Catalase; Quercetin; NF-KB; Bax; Caspace3; MDA; Age, Bcl2; Apoptosis
• ISSN: 2175-9790; 1984-8250; 2175-9790
• DOI: 10.1590/s2175-979020200003180861

Adverse changes occur gradually in the skeletal muscles with age via continuous exposure to oxidative stress. Quercetin, a member of the flavonoids family, possesses anti-oxidative and radical-scavenging activities. Therefore, this study investigated the role of quercetin to modulate age-induced changes in the transcript levels of some apoptosis-related genes in rat’s gastrocnemius muscles, up to 15 months-old. Half of the rats at each age (1, 5, 10 and 15 months old) were given a vehicle and the other half was given 200 mg/kg quercetin for 2 weeks, respectively. With the increase of age, vehicle groups showed hyalinization of the muscle fibers and a decrease of the catalase and an increase of the malondialdehyde levels. Down-regulation of Bcl2 gene and up-regulation of both NF-κB and Bax genes were recorded. Interestingly, quercetin groups showed focal hyalinization of the muscle fibers at both 10th and 15th months old. An increase in the catalase and a decrease in malondialdehyde levels, up-regulation of Bcl2 gene and down-regulation of both NF-κB and Bax genes were recorded. In conclusion, quercetin minimized age-induced alteration in the morphological structure and the expression of the apoptosis-related genes via increasing the antioxidant defense in the gastrocnemius muscle.