The Effect Of Astaxanthin On Neuropathic Pain In Rats Through Inducing HO-1

Objective:Tudy the Effects of Astaxanthin on the Behavioral,Oxidative Stress and Inflammatory Responses of Rats with Neuropathic Pain Caused by Chronic Constriction Injury(CCI)and Investigate Its Mechanism of Action.Methods: Seventy-two adult male Sprague-Dawley rats,weighing 200 to 250 g,are randomly divided into six groups(n=12): model group(CCI),AST treated group,Znpp + AST group,solvent group(DMSO),Sham surgery group and normal control group.The rat chronic neuropathic pain model is prepared by CCI method in all groups except the normal control group,and the DMSO group,AST group and Znpp+AST group are injected with DMSO(0.5%,10ul),AST(1ug,10ul),Znpp(24ug,10ul)+ AST(1ug,10ul)once daily in the sheath for 5 days after surgery,respectively.The lumbar spinal cord(L4-L6)is taken at 14 d after surgery.Western blot method is used to detect changes in HO-1 protein content,enzyme-linked immunosorbent assay(ELISA)is used to detect superoxide dismutase(SOD),glutathione peroxidase(GSH-PX)expression levels and tumor necrosis factor(TNF-?)and interleukin IL-1?(IL-1?)content in the lumbar spinal cord of rats.Immunofluorescence double staining is used to determine the expression of HO-1 in each group.Results : Compared with Control group,CCI rats has significantly lowered PWMT and PWTL(P<0.05)in 7~14 days after surgery,elevated spinal cord HO-1expression level and TNF-?,IL-1? expression,and decreased SOD,GSH-PX expression(P<0.05)in 14 days after surgery;compared with CCI group,AST grouphas elevated PWMT,PWTL(P<0.05)in 7-14 days after surgery,decreased TNF-?,1L-1? expression,elevated SOD,GSH-PX expression,and significantly elevated spinal cord HO-1 expression level(P<0.05)in 7~14d after surgery postoperatively;while Znpp+AST group has reversed the expression results of AST group.Conclusion: Astaxanthin can alleviate neuropathic pain in CCI rats.Its mechanism is related to the induction of HO-1expression in the spinal cord,reduced release of inflammatory factors TNF-? and IL-1?;and inhibition of oxidative stress response.