Pistachio hull polysaccharide protects Nile tilapia against LPS-induced excessive inflammatory responses and oxidative stress, possibly via TLR2 and Nrf2 signaling pathways.

Polysaccharides are polymeric carbohydrates found in living organisms, which have several physiological functions. In the present study, Nile tilapia (Oreochromis niloticus) were fed diets containing three levels (0%, 0.2%, and 0.6%) of Pistacia vera hull polysaccharide (PHP) for 45 days and then injected with PBS or bacterial lipopolysaccharide (LPS). Before the LPS challenge, Nile tilapia fed 0.2% and 0.6% PHP showed significantly increased mean final weight and weight gain compared to those received 0% PHP. The specific growth rate and feed conversion ratio were significantly improved in the treatment fed 0.6% PHP compared to the remaining groups. After LPS challenge, the activities of liver antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase exhibited the highest values in the 0.6% PHP group. Malondialdehyde (MDA) levels were significantly augmented in the model (fed 0% PHP diet and injected with LPS) and 0.2% PHP groups compared to the control. However, MDA showed decreased levels in the 0.6% PHP group. LPS induced higher mRNA and/or protein levels of Toll-like receptor 2 (TLR2), nuclear factor kappa B (NF-κB), myeloid differentiation primary response protein 88 (Myd88), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interferon γ (IFN-γ) in Nile tilapia liver. However, PHP administration significantly upregulated the expression of interleukin 10 (IL-10), nuclear erythroid 2-related factor 2 (Nrf2), SOD, and CAT, but markedly suppressed TLR2, NF-κB, Myd88, and pro-inflammatory cytokine expression and/or production in the liver. The findings of the current study indicated that PHP has positive effects on growth performance, immune gene-related expression, and antioxidative activities. We can conclude that PHP can attenuate LPS-induced oxidative stress and inflammatory responses in vivo, possibly via induction of Nrf2 and blockade of TLR2/Myd88/NF-κB pathways in Nile tilapia.