Efficacy of tubing technique with biomaterials compared to direct coaptation technique after peripheral neurotmesis in nerve healing and return to functionality in young adult rats: a systematic review protocol.

BACKGROUND: Peripheral nerves are constant targets of traumatic injury which may result in neurotmesis and which invariably requires surgical treatment. In view of this, tissue engineering studies developed biomaterials which were first tested in animal models and used as a guide for nerve stumps in the procedure in order to speed up the healing process. Therefore, the aim of this study is to evaluate the efficacy of biomaterials used in tubing technique on healing and histological and functional recovery after peripheral nerve neurotmesis in rats. METHODS: We will search PubMed/MEDLINE, Embase, Web of Science, LILACS, and CENTRAL (from inception onwards). Grey literature will be identified through searching dissertation databases, guidelines, policy documents, and reports. We will include randomized and non-randomized trials conducted in young adult rats with peripheral neurometsis undergoing surgical repair through tubing technique with biomaterials. Primary outcomes will be histomorphometry, immunohistochemistry of the nerve tissue, and sciatic functional index. Secondary outcome will be nerve macroscopic evaluation. Two reviewers will independently screen all citations, full-text articles, and abstract data. Potential conflicts will be resolved through discussion. The methodological quality (or risk of bias) of individual studies will be appraised using an appropriate tool. If feasible, we will conduct random effects meta-analysis. DISCUSSION: This systematic review of animal studies will identify, evaluate, and synthetize the evidence on the the efficacy of tubing technique with biomaterials compared to direct coaptation technique after peripheral neurotmesis in nerve healing and return to functionality. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42018106042.

Preventive role of metformin on peripheral neuropathy induced by diabetes.

Metformin is the first line drug in the treatment of type 2 diabetes, however, little is known about its therapeutic potential to prevent or delay damage to the peripheral nerve. Thus, the aim of this study was to investigate whether metformin is able to attenuate the neuroinflammatory response in sciatic nerve of insulin-dependent diabetic mice. Swiss Webster mice were divided into four groups: Control, Diabetic (STZ), Diabetic +100 mg/kg/day of metformin (STZ + M100) and Diabetic +200 mg/kg/day of metformin. Diabetes was induced by streptozotocin (90 mg/kg, i.p.). Only animals with glycemia ≥270 mg/dl were considered diabetics. Metformin prevented atrophy of myelinated axons, and reduced expression of inflammatory mediators (interleukin-1ß, inducible nitric oxide synthase and nitric oxide). However, treatment with 200 mg of metformin was more effective in increasing neurotrophic (myelin basic protein and neural growth factor), angiogenic (vascular endothelial growth factor) and anti-inflammatory (inhibitor kappa B-alpha and interleukin 10) factors. Thus, metformin treatment, especially at the dose of 200 mg, protected the nerve from damages related to chronic hyperglycemia.