Objective:To observe the deregulation of autophagy in diabetic peripheral neuropathy(DPN) and investigate whether Jinmaitong(筋脉通i,JMT) alleviates DPN by inducing autophagy.Methods:DPN models were established by streptozotocin-induced diabetic rats and Schwann cells(SCs) cultured in high glucose medium.The pathological morphology was observed by the improved Bielschowsky’s nerve fiber axonal staining and the Luxol fast blue-neutral red myelin staining.The ultrastructure was observed by the transmission electron microscopy.Beclinl level was detected by immunohistochemistry and Western blot.The proliferation of cultured SCs was detected by methylthiazolyldiphenyl-tetrazolium bromide.Results:Diabetic peripheral nerve tissues demonstrated pathological morphology and reduced autophagic structure,accompanied with down-regulation of Beclinl.JMT apparently alleviated the pathological morphology change and increased the autophagy[in vivo,Beclinl integral optical density(IOD) value of the control group 86.6±17.7,DM 43.9±8.8,JMT 73.3 ±17.8,P<0.01 or P<0.05,in vitro Beclinl IOD value of the glucose group 0.4710.25 vs the control group 0.88 ±0.29,P<0.05].Consequently,inhibition of autophagy by 3-methyladenine resulted in a time- and concentrationdependent decrease of the proliferation of SCs(P<0.05,P<0.01).Conclusions:Down-regulation of autophagy in SCs might contribute to the pathogenesis of DPN.JMT alleviates diabetic peripheral nerve injury at least in part by inducing autophagy. Objective: To observe the deregulation of autophagy in diabetic peripheral neuropathy (DPN) and RESEARCH whether Jinmaitong (JMT) alleviates DPN by inducing autophagy. Methods: DPN models were established by streptozotocin-induced diabetic rats and Schwann cells ) cultured in high glucose medium. The pathological morphology was observed by the improved Bielschowsky’s nerve fiber axonal staining and the Luxol fast blue-neutral red myelin staining. The ultrastructure was observed by the transmission electron microscopy. Beeclone level was detected by immunohistochemistry and Western blot . The proliferation of cultured SCs was detected by methylthiazolyldiphenyl-tetrazolium bromide. Results: Diabetic peripheral tissues showing pathological morphology and reduced autophagic structure, accompanied with down-regulation of Beclinl. JMT apparently alleviated the pathological morphology change and increased the autophagy [in vivo , Beclinl integral optical density (IOD) value of the c ontrol group 86.6 ± 17.7, DM 43.9 ± 8.8, JMT 73.3 ± 17.8, P <0.01 or P <0.05, in vitro Beclinl IOD value of the glucose group 0.4710.25 vs. the control group 0.88 ± 0.29, P <0.05] , inhibition of autophagy by 3-methyladenine resulted in a time- and concentration dependent decrease of the proliferation of SCs (P <0.05, P <0.01) .Conclusions: Down-regulation of autophagy in SCs might contribute to the pathogenesis of DPN. JMT alleviates diabetic peripheral nerve injury at least in part by inducing autophagy.