Abstract： Objective To investigate the mechanism of nerve growth factor β(NGF β)in diabetic peripheral neuropathy(DPN).Methods High glucose cell model was established and divided into control group,OE-NGFβ group and NC-NGFβ group.Diabetic neuropathy model was established and divided into rat control group,OE-NGFβ group and NC-NGFβ group.RT-qPCR and Western blot were used to detect the expression changes of insulin-like growth factor-1(IGF-1),intercellular adhesion molecule-1(ICAM-1),tumor necrosis factor-α(TNF-α),autophagy-related gene 12(ATG12),microtubule-associated protein 1A/1B light chain 3B(LC3B)and P62 in cells and rat sciatic nerves.The levels of malondialdehyde(MDA),nitric oxide(NO),reactive oxygen species(ROS)and superoxide dismutase(SOD)in blood samples of DPN rats were detected by ELISA.Results Compared with control group,the mRNA and protein levels of IGF-1,ATG12,LC3B and P62 in the OE-NGFβ group were significantly increased(P<0.001),while the mRNA and protein levels of ICAM-1 and TNF-α were significantly decreased(P<0.001).Compared with control group,the mRNA and protein levels of IGF-1,ATG12,LC3B and P62 in the sciatic nerve of the rat OE-NGFβ group were sig-nificantly increased(P<0.001),and the mRNA and protein levels of ICAM-1 and TNF-α were significantly decreased(P<0.001).In addition,compared with control group,the levels of MDA,NO,and ROS were significantly decreased(P<0.001)and the levels of SOD were significantly increased(P<0.001)in the rat OE-NGFβ group.Conclusion NGFβ may exert neuroprotective effects in DPN by regulating autophagy and antioxidant,suggesting that NGFβ may be a potential therapeutic target for DPN.