Seaweed-Derived Polysaccharides Attenuate Heat Stress-Induced Splenic Oxidative Stress and Inflammatory Response via Regulating Nrf2 and NF-κB Signaling Pathways.
Wen-Chao LiuDi-Pai ZhuangYue ZhaoBalamuralikrishnan BalasubramanianZhi-Hui ZhaoPublished in: Marine drugs (2022)
With global warming, heat stress (HS) has become a worldwide concern in both humans and animals. The ameliorative effect of seaweed ( Enteromorpha prolifera ) derived polysaccharides (SDP) on HS-induced oxidative stress and the inflammatory response of an immune organ (spleen) was evaluated using an animal model ( Gallus gallus domesticus ). In total, 144 animals were used in this 4-week trial and randomly assigned to the following three groups: thermoneutral zone, HS, and HS group supplemented with 1000 mg/kg SDP. Dietary SDP improved the antioxidant capacity and reduced the malondialdehyde (MDA) of the spleen when exposed to HS, regulated via enhancing nuclear factor erythroid 2-related factor-2 (Nrf2) signaling. Furthermore, the inclusion of SDP reduced the levels of pro-inflammatory cytokines and alleviated HS-induced splenic inflammatory response by suppressing the nuclear factor-kappa B (NF-κB) p65 signaling. These findings suggest that the SDP from E. prolifera can be used as a functional food and/or feed supplement to attenuate HS-induced oxidative stress and inflammatory responses of the immune organs. Moreover, the results could contribute to the development of high-value marine products from seaweed for potential use in humans and animals, owing to their antioxidant and anti-inflammatory effects.
Keyphrases
- nuclear factor
- inflammatory response
- toll like receptor
- oxidative stress
- heat stress
- lps induced
- stress induced
- lipopolysaccharide induced
- diabetic rats
- signaling pathway
- hydrogen peroxide
- clinical trial
- heat shock
- ischemia reperfusion injury
- anti inflammatory
- study protocol
- immune response
- nitric oxide
- randomized controlled trial
- pi k akt
- human health
- climate change
- phase ii
- phase iii
- epithelial mesenchymal transition
- cell death
- open label
- cell cycle arrest