Improvement of diabetes-induced spinal cord axon injury with taurine via nerve growth factor dependent Akt/mTOR pathway

Abstract

Abstract As a common nervous system disorder, Diabetic neuropathy (DN) is caused by diabetes mellitus (DM). According to evidences, axonal degeneration is a main pathological feature of diabetic peripheral neuropathy, and taurine may be a protective candidate. But, the beneficial effect of taurine on spinal cord axon injury (SCAI) in DN and its regulatory mechanism is rarely exhibited in reports. In this study, as demonstrated by our results, taurine greatly improved abnormal axonal morphology of spinal cord (SC) and nerve function in diabetic rats induced by streptozotocin (STZ), and induced neurite outgrowth of cerebral cortex neurons with high glucose exposure. Moreover, taurine up-regulated expression of nerve growth factor (NGF) and neurite outgrowth relative protein GAP-43 in the SC of diabetic rats, as well as the cerebral cortex neurons or the VSC4.1 cells with high glucose exposure. Besides, taurine increased the phosphorylation levels of TrkA, Akt, and mTOR. Also, in the presences of NGF-neutralizing antibody and Akt or mTOR inhibitors, beneficial effects of taurine could be blocked. As suggested by these results, taurine can promote SC axon repair in diabetic rats, with the mechanism partly associated with NGF-dependent activation of Akt/mTOR pathway. According to our findings, the role of taurine in improving SCAI of DN and its mechanism is clarified.