Chondroitin sulfate(CS)has some physiological activities such as anti-inflammatory and immune regulation.But there are few reports on fish as animal model.This experiment was conducted to investigate the effects of CS on serum antioxidant and immune indexes and expression of immune related genes in different organs of Schizothorax prenanti under cadmium stress.In this study,we investigated the effect of CS on serum antioxidant and immune indexes and expression of immune related genes in different organization of Schizothorax prenanti under cadmium stress.CS(0.2%,0.4%,0.8%)were added to the diet and the fish was fed for 6 weeks.The effects of growth indicators,serum biochemical indexes,immune indexes and expression of related genes in head kidney,spleen,liver and midgut were measured.The fish were exposed to 0.1mg/L cadmium for 1d,7d,14 d and 21 d to determine the serum biochemical indexes and the expression of related genes of organization under cadmium stress for 21 d.The experimental results are as follows:1.Different doses of CS significantly increased the weight gain rate,specific growth rate and muscle protein content of Schizothorax prenanti,but there were no significant effect on condition factor and fasting fat index,as well as muscle moisture,ash and fat content.2.0.8% CS significantly decreased MDA and Ig M contents in Schizothorax prenanti.0.4% CS significantly increased the activity of GSH-Px and GSH-ST and decreased the content of serum cortisol.The contents of NO,GPT,TG and i NOS activity in serum of Schizothorax prenanti were significantly decreased,while the contents of HDL-C in serum of Schizothorax prenanti were significantly increased.In addition,0.4% CS and 0.8% CS significantly reduced the serum LDL-C content of Schizothorax prenanti.The schizothorax Prenanti were exposed to 0.1 mg/L cadmium solution for 1,7,14 and 21 days,compared with the control group,the cadmium stress group significantly increased the content of MDA,NO and the activity of GPT,GPT and i NOS,and significantly decreased the activity of GSH-Px,GSH-ST and SOD in the serum of Schizothorax prenanti,while all the doses of CS could improve the oxidative stress caused by cadmium to different degrees and protect the body from oxidative damage.Moreover,cadmium exposure for 21 days could significantly increase the contents of cadmium in liver,midgut and muscle of Schizothorax Prenanti,while CS decreased the accumulation of cadmium in tissues of Schizothorax Prenanti.3.0.4% CS and 0.8% CS can significantly up-regulate the expression of pro-inflammatory factors(IL-8,IL-10,TNF-α)and anti-inflammatory cytokines(IL-10,TGF-β)of TLR pathway,and activate the TLR pathway to improve the immune performance of the body.0.4% CS and 0.8% CS can activate MDA5 pathway and downstream molecules(LGP and IRF7),and play an important role in inhibit cell apoptosis.0.4% CS and 0.8% CS could up-regulated the expression of PI3 K and AKT genes in body tissues.In addition,CS0.4 inhibits STAT and downstream signaling molecules to enhance immune response of body.4.Cadmium stress induced a strong early immune response.At the same time,TLR signaling pathway was activated,and the up-regulation of pro-inflammatory cytokines(IL-8,IL-10,TNF-α)caused inflammatory response.And 0.4% CS and 0.8% CS could improve the immune inflammatory response caused by cadmium.Cadmium can activate MDA5 pathway and apoptosis pathway in the tissues of Schizothorax prenanti,and 0.4% CS and0.8% CS can inhibit the activation of this pathway and protect the body from damage.CS can activate the PI3K/AKT signaling pathway and inhibit STAT and its downstream related genes to improve the damage caused by cadmium stress,0.4 % CS and 0.8% CS show better immune regulation ability.Therefore,0.4% CS and 0.8% CS reduced the release of cadmium-induced inflammatory cytokines in Schizothorax Prenanti tissues by inhibiting the TLR pathway.In addition,0.4% CS can inhibit cell apoptosis and STAT and its downstream related genes by activating the PI3K/AKT signaling pathway,effectively protect Schizothorax Prenanti from oxidative damage. |