title: Improved neural microcirculation and regeneration after peripheral nerve decompression in DPN rats.
abstract: OBJECTIVE
  Recently, neural microcirculation and regeneration were regarded as critical factors in diabetic peripheral neuropathy (DPN) improvement. In the present study, we explored the cytological and molecular mechanisms how peripheral nerve decompression impaired nerve injury.
  
  
  METHODS
  Forty-five male SD rats were established as the DPN model. HE staining was used to observe the morphology and distribution of microvessels. Transmission electron microscopy was applied to observe the morphology and distribution of Schwann cells. Immunohistochemical staining was performed to measure nerve growth factor (NGF), tyrosine kinase receptor A (TrkA) and growth-associated protein 43 (GAP-43) in the distal sciatic nerve.
  
  
  RESULTS
  Distribution of microvessels and Schwann cells decreased in the DPN group (p < 0.05). NGF, TrkA and GAP-43 also decreased significantly in the DPN group (p < 0.05). NGF, TrkA, GAP-43 and distribution of microvessels and Schwann cells increased in the decompressed group (p < 0.05).
  
  
  CONCLUSIONS
  In DPN rats, after nerves are compressed, microcirculation disturbance and hypoxia ischemia will happen, which cause decreased expression of NGF, TrkA and GAP-43. Finally, the self-healing function of compressed nerves is impacted. Conversely, nerve decompression can improve neural microcirculation and regeneration and change the former pathological process.
authors.affiliation: a Department of Neurosurgery , Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.
authors.forename: Wenxiang
authors.initials: W
authors.lastname: Zhong
authors.affiliation: a Department of Neurosurgery , Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.
authors.forename: Min
authors.initials: M
authors.lastname: Yang
authors.affiliation: a Department of Neurosurgery , Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.
authors.forename: Wenchuan
authors.initials: W
authors.lastname: Zhang
authors.affiliation: b Institute of Neurosurgery, Policlinico Gemelli, Catholic University School of Medicine , Rome , Italy.
authors.forename: Massimiliano
authors.initials: M
authors.lastname: Visocchi
authors.affiliation: c Department of Neurology , Huashan Hospital, Affiliated to Fudan University , Shanghai , China.
authors.forename: Xiangjun
authors.initials: X
authors.lastname: Chen
authors.affiliation: a Department of Neurosurgery , Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine , Shanghai , China.
authors.forename: Chenlong
authors.initials: C
authors.lastname: Liao
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000473:pathology / Q000503:physiopathology; D003929:Diabetic Neuropathies / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D004195:Disease Models, Animal; D019922:GAP-43 Protein / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D008833:Microcirculation / Q000502:physiology*; D046529:Microscopy, Electron, Transmission; D055806:Microvessels / Q000473:pathology / Q000502:physiology; D009408:Nerve Compression Syndromes / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy*; D020932:Nerve Growth Factor / Q000378:metabolism; D009416:Nerve Regeneration / Q000502:physiology*; D011897:Random Allocation; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000378:metabolism; D012583:Schwann Cells / Q000378:metabolism / Q000473:pathology; D012584:Sciatic Nerve / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology
chemical_list: D019922:GAP-43 Protein; D020932:Nerve Growth Factor; D020917:Receptor, trkA
keywords: Diabetic peripheral neuropathy; Schwann cell; growth-associated protein 43 (GAP-43); microcirculation; nerve decompression; nerve growth factor (NGF); tyrosine kinase receptor A (TrkA)