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Neurochem.<\/jats:italic>\n                      (2012)\n                      <jats:bold>121<\/jats:bold>\n                      , 818\u2013829.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>The disruption of blood\u2013spinal cord barrier (BSCB) after spinal cord injury (SCI) elicits an intensive local inflammation by the infiltration of blood cells such as neutrophils and macrophages, leading to cell death and permanent neurological disability. SCI activates matrix metalloprotease\u20109 (MMP\u20109), which is known to induce BSCB disruption. Here, we examined whether valproic acid (VPA), a histone deacetylase inhibitor, would attenuate BSCB disruption by inhibiting MMP\u20109 activity, leading to improvement of functional outcome after SCI. After moderate spinal cord contusion injury at T9, VPA (300\u2003mg\/kg) were immediately injected subcutaneously and further injected every 12\u2003h for 5\u2003days. Our data show that VPA inhibited MMP\u20109 activity after injury, and attenuated BSCB permeability and degradation of tight junction molecules such as occludin and ZO\u20101. In addition, VPA reduced the expression of inflammatory mediators including tumor necrosis factor\u2010\u03b1. Furthermore, VPA increased the levels of acetylated histone 3, pAkt, and heat\u2010shock protein 27 and 70, which have anti\u2010apoptotic functions after SCI. Finally, VPA inhibited apoptotic cell death and caspase 3 activation, reduced the lesion volume and improved functional recovery after injury. Thus, our results demonstrated that VPA improves functional recovery by attenuating BSCB disruption via inhibition of MMP\u20109 activity after SCI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/j.1471-4159.2012.07731.x","type":"journal-article","created":{"date-parts":[[2012,3,12]],"date-time":"2012-03-12T14:28:50Z","timestamp":1331562530000},"page":"818-829","source":"Crossref","is-referenced-by-count":107,"title":["Valproic acid attenuates blood\u2013spinal cord barrier disruption by inhibiting matrix metalloprotease\u20109 activity and improves functional recovery after spinal cord injury"],"prefix":"10.1111","volume":"121","author":[{"given":"Jee Y.","family":"Lee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hwang S.","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hye Y.","family":"Choi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tae H.","family":"Oh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bong G.","family":"Ju","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tae Y.","family":"Yune","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,4,2]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1824"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.21-19-07724.2001"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1089\/neu.1995.12.1"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1089\/neu.2000.17.915"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0955-0674(99)80046-5"},{"key":"e_1_2_7_7_1","first-page":"395","article-title":"Histone deacetylase inhibitors sodium butyrate and valproic acid delay spontaneous cell death in purified rat retinal ganglion cells","volume":"17","author":"Biermann J.","year":"2011","journal-title":"Mol. 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