Jinmaitong alleviates the diabetic peripheral neuropathy by inducing autophagy

To observe the deregulation of autophagy in diabetic peripheral neuropathy (DPN) and investigate whether Jinmaitong (c < eparts per thousand eEuroe, JMT) alleviates DPN by inducing autophagy. 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. Beclin1 level was detected by immunohistochemistry and Western blot. The proliferation of cultured SCs was detected by methylthiazolyldiphenyl-tetrazolium bromide. Diabetic peripheral nerve tissues demonstrated pathological morphology and reduced autophagic structure, accompanied with down-regulation of Beclin1. JMT apparently alleviated the pathological morphology change and increased the autophagy [in vivo, Beclin1 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 Beclin1 IOD value of the glucose group 0.47 +/- 0.25 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). 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.