Altered Expression of Matrix Metalloproteinases and Tight Junction Proteins in Rats following PEMF-Induced BBB Permeability Change

Objective To investigate the expression of occludin,ZO‐1,MMP‐2,and MMP‐9 in cerebral microvasculature following Pulse Electromagnetic Field（PEMF） induced BBB permeability change.Methods Sprague‐Dawley rats were randomized into PEMF and sham exposed groups（n=8）.After exposure to PEMF at 0.5,1,3,6,and 12 h,BBB permeability was measured by Evans‐Blue extravasation.The expression of occludin,ZO‐1,MMP‐2,and MMP‐9 were detected by real‐time quantitative reverse transcriptase PCR and western blotting.MMP‐2 and MMP‐9 activity were detected by EnzChek gelatinase assay.Results Compared with the sham group,PEMF exposure led to increased permeability of the BBB to EB,which was prolonged after exposure.BBB permeability became progressively more severe,and recovered at 6 h.The gene and protein expression of occludin and ZO‐1 were significantly decreased,while MMP‐2 and MMP‐9 expression were significantly increased after exposure to PEMF.All levels of expression recovered 12 h following PEMF.Conclusion Changes to BBB permeability were related to the alteration expression of tight junction proteins and matrix metalloproteinase after exposure to PEMF.

Basic research and clinical progress of sepsis-associated encephalopathy

Sepsis-associated encephalopathy(SAE),a major cerebral complication of sepsis,occurs in 70%of patients admitted to the intensive care unit(ICU).This condition can cause serious impairment of consciousness and is associated with a high mortality rate.Thus far,several experimental screenings and radiological techniques(e.g.,electroencephalography)have been used for the non-invasive assessment of the structure and function of the brain in patients with SAE.Nevertheless,the pathogenesis of SAE is complicated and remains unclear.In the present article,we reviewed the currently available literature on the epidemiology,clinical manifestations,pathology,diagnosis,and management of SAE.However,currently,there is no ideal pharmacological treatment for SAE.Treatment targeting mitochondrial dysfunction may be useful in the management of SAE.