Matrix metalloproteinase 3 is one of matrix metalloproteinase family members, which degrades a wide range of components of the extracellular matrix and participates in tissue morphogenesis, wound healing and inflammation. In addition, matrix metalloproteinase 3 is involved in pathogenesis and progress of a spectrum of diseases and malignant tumors, such as rheumatic arthritis, arteriosclerosis, breast cancer, and so on. Recent studies have demonstrated that matrix metalloproteinase 3 may be a novel signaling proteinase from apoptotic neuronal cells to microglia, which results in degeneration of neurons in Alzheimer's disease and Parkinson's disease by activating microglia. There is also an association between genetic polymorphisms of matrix metalloproteinase 3 at promoter region 5A/6A and susceptibility of myocardial infarction. Decrease in serum concentration of matrix metalloproteinase 3 after myocardial infarction may be a useful parameter for diagnosing sudden death due to myocardial infarction in forensic practice. Expression of matrix metalloproteinase 3 varies with different types of brain injuries, suggesting that it may contribute to synaptic plasticity during functional recovery. To elucidate the time-dependent expression of matrix metalloproteinase 3 may provide a new way for wound age determination in the brain.

Objective This study aims to evaluate the changes of Cdk5 expression at the time of 3 hours to 10 days after moderate brain injury by blunt force impact in a rat model,and to demonstrate its forensic significance.Methods To establish a rat model of blunt focal brain contusion,and to observe the changes of Cdk5 expression in brain tissue at different timepoints after brain injury by immunohistochemistry and Western blot.Results A low expression level of Cdk5 was observed in the brain tissue of both normal and sham control groups.The expression of Cdk5 increased after 3 and 6 hours,remarkably increased at 12 hours,and reached the maximal level at 24 hours after focal brain injury.The Cdk5 level gradually decreased 3 days,5 days,7 days,and 10 days and reached the normal level 7 and 10 days after the injury,with no statistical difference (P＞0.05) compared with the normal and sham control groups.Conclusion The expression of Cdk5 increased in the peripheral area of contusion tissue after blunt brain injury in rats,showing single peak change,and dropped to normal level with the time extension.The change of Cdk5 expression may provide a new reference index for the prediction of early brain contusion.

Background: The mechanism of peripheral axon transport in neuropathic pain is still unclear. Chemokine ligand 13 (CXCL13) and its receptor (C-X-C chemokine receptor type 5, CXCR5) as well as GABA transporter 1 (GAT-1) play an important role in the development of pain. The aim of this study was to explore the axonal transport of CXCL13/CXCR5 and GAT-1 with the aid of the analgesic effect of botulinum toxin type A (BTX-A) in rats. Methods: Chronic constriction injury (CCI) rat models were established. BTX-A was administered to rats through subcutaneous injection in the hind paw. The pain behaviors in CCI rats were measured by paw withdrawal threshold and paw withdrawal latencies. The levels of CXCL13/CXCR5 and GAT-1 were measured by western blots. Results: The subcutaneous injection of BTX-A relieved the mechanical allodynia and heat hyperalgesia induced by CCI surgery and reversed the overexpression of CXCL13/CXCR5 and GAT-1 in the spinal cord, dorsal root ganglia (DRG), sciatic nerve, and plantar skin in CCI rats. After 10 mmol/L colchicine blocked the axon transport of sciatic nerve, the inhibitory effect of BTX-A disappeared, and the levels of CXCL13/CXCR5 and GAT-1 in the spinal cord and DRG were reduced in CCI rats. Conclusions BTX-A regulated the levels of CXCL13/CXCR5 and GAT-1 in the spine and DRG through axonal transport. Chemokines (such as CXCL13) may be transported from the injury site to the spine or DRG through axonal transport. Axon molecular transport may be a target to enhance pain management in neuropathic pain.