穿心莲内酯调节神经调节蛋白1对大鼠脊髓损伤的作用及机制OA

Objective:To explore the effect and mechanism of andrographolide on spinal cord injury in rats based on the Nrg1/ErbB2 pathway.Methods:Among 72 rats,12 rats were randomly selected as the nor-mal group,and the rest rats were used to establish a spinal cord injury model and assigned into spinal cord in-jury group,L-andrographolide group,M-andrographolide group,H-andrographolide group,and androgra-pholide+AG-825(ErbB2 inhibitor)group,with 12 rats in each group,and treated for 28 days.Enzyme linked immunosorbent assay(ELISA)was performed to detect the levels of inflammatory factors in the spinal cord of rats.The BBB scale was used to evaluate the recovery of hind limb motor function in rats.HE and Nissl staining were used to measure morphological changes in spinal cord tissue.Luxol Fast Blue(LFB)stai-ning was performed to measure demyelination at the site of spinal cord injury.In addition,Western blot was performed to detect the expression of Nrg1 and ErbB2 proteins in spinal cord tissue.Results:Compared with the normal group,the spinal cord injury group exhibited lesion cavities,demyelination,and inflammatory cell infiltration at the injury site.The levels of TNF-α,IL-1β,and IL-6 were increased,while the BBB score,ErbB2 and Nrg1 protein expression,and the number of Nissl positive cells were all decreased(P＜0.05).Compared with the spinal cord injury group,the L-andrographolide group,M-andrographolide group,and H-andrographolide group showed reduced demyelination at the injury site,the levels of TNF-α,IL-1 β,and IL-6 were decreased sequentially,while the BBB score,number of Nissl positive cells,ErbB2 and Nrg1 protein expression were increased in a dose-dependent manner(P＜0.05).Compared with the H-andrographolide group,the andrographolide+AG-825 group had aggravated spinal cord injury,the levels of TNF-α,IL-1β,and IL-6 were increased,while the BBB score,number of Nissl positive cells,ErbB2 and Nrg1 protein ex-pression were decreased(P＜0.05).Conclusion:Andrographolide improves spinal cord injury in rats by acti-vating the Nrg1/ErbB2 signaling pathway.