{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,3]],"date-time":"2026-03-03T06:22:22Z","timestamp":1772518942235,"version":"3.50.1"},"reference-count":55,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,2,13]],"date-time":"2013-02-13T00:00:00Z","timestamp":1360713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Tumor necrosis factor\u2010\u03b1 (TNF) plays a prominent role in the brain damage and functional deficits that result from ischemic stroke. It was recently reported that the thalidomide analog 3,6\u2032\u2010dithiothalidomide (3,6\u2032\u2010DT) can selectively inhibit the synthesis of TNF in cultured cells. We therefore tested the therapeutic potential of 3,6\u2032\u2010DT in a mouse model of focal ischemic stroke. Administration of 3,6\u2032\u2010DT immediately prior to a stroke or within 3 hr after the stroke reduced infarct volume, neuronal death, and neurological deficits, whereas thalidomide was effective only when administered prior to stroke. Neuroprotection was accompanied by decreased inflammation; 3,6\u2032\u2010DT\u2010treated mice exhibited reduced expression of TNF, interleukin\u20101\u03b2, and inducible nitric oxide synthase; reduced numbers of activated microglia\/macrophages, astrocytes, and neutrophils; and reduced expression of intercellular adhesion molecule\u20101 in the ischemic brain tissue. 3,6\u2032\u2010DT treatment attenuated stroke\u2010induced disruption of the blood\u2013brain barrier by a mechanism that appears to involve suppression of matrix metalloproteinase\u20109 and preservation of occludin. Treatment with 3,6\u2032\u2010DT did not reduce ischemic brain damage in mice lacking TNF receptors, consistent with a critical role for suppression of TNF production and TNF signaling in the therapeutic action of 3,6\u2032\u2010DT. These findings suggest that anti\u2010inflammatory mechanisms underlie the therapeutic actions of 3,6\u2010DT in an animal model of stroke. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jnr.23190","type":"journal-article","created":{"date-parts":[[2013,2,13]],"date-time":"2013-02-13T12:04:10Z","timestamp":1360757050000},"page":"671-680","source":"Crossref","is-referenced-by-count":36,"title":["3,6\u2032\u2010dithiothalidomide improves experimental stroke outcome by suppressing neuroinflammation"],"prefix":"10.1002","volume":"91","author":[{"given":"Jeong Seon","family":"Yoon","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jong\u2010Hwan","family":"Lee","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David","family":"Tweedie","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohamed 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