Effects of Heat-Induced Oxidative Stress and Astaxanthin on the NF-kB , NFE2L2 and PPARα Transcription Factors and Cytoprotective Capacity in the Thymus of Broilers.
Donna Lee KuehuYuanyuan FuMasaki NasuHua YangVedbar S KhadkaYouping DengPublished in: Current issues in molecular biology (2024)
The thymus, a central lymphoid organ in animals, serves as the site for T cell development, differentiation and maturation, vital to adaptive immunity. The thymus is critical for maintaining tissue homeostasis to protect against tumors and tissue damage. An overactive or prolonged immune response can lead to oxidative stress from increased production of reactive oxygen species. Heat stress induces oxidative stress and overwhelms the natural antioxidant defense mechanisms. This study's objectives were to investigate the protective properties of astaxanthin against heat-induced oxidative stress and apoptosis in the chicken thymus, by comparing the growth performance and gene signaling pathways among three groups: thermal neutral, heat stress, and heat stress with astaxanthin. The thermal neutral temperature was 21-22 °C, and the heat stress temperature was 32-35 °C. Both heat stress groups experienced reduced growth performance, while the astaxanthin-treated group showed a slightly lesser decline. The inflammatory response and antioxidant defense system were activated by the upregulation of the NF-kB , NFE2L2 , PPARα , cytoprotective capacity, and apoptotic gene pathways during heat stress compared to the thermal neutral group. However, expression levels showed no significant differences between the thermal neutral and heat stress with antioxidant groups, suggesting that astaxanthin may mitigate inflammation and oxidative stress damage.
Keyphrases
- heat stress
- oxidative stress
- heat shock
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- dna damage
- inflammatory response
- signaling pathway
- immune response
- reactive oxygen species
- insulin resistance
- transcription factor
- hydrogen peroxide
- lps induced
- adipose tissue
- cell death
- type diabetes
- copy number
- cell proliferation
- lipopolysaccharide induced
- fatty acid
- toll like receptor
- pi k akt
- binding protein
- endoplasmic reticulum stress
- dendritic cells
- metabolic syndrome
- newly diagnosed