| Stroke is a major cause of hospitalization, chronic disability and death. Prompt reperfusion of ischemic brain tissue is critical for restoring normal function. However, this return of blood flow can paradoxically produce a progressive destruction of reversibly damaged cells, thereby leading to tissue dysfunction and infarction. This "reperfusion injury" has a multifactorial etiology but appears to be strongly associated with an inflammatory response. Inflammation in the ischemic brain and its role in neurotoxicity is presently an area of considerable interest, which may lead to the identification of new therapeutic targets for patients suffering ischemic brain injury. Tumor necrosis factor related apoptosis induced ligand (TRAIL) is a member of the tumor necrosis factor (TNF) superfamily. The role of TRAIL in cerebral ischemia-reperfusion injury has never been covered in detail. In the present study we investigated whether the TRAIL-DR5 signaling system could be involved in ischemia-reperfusion-induced brain injury.Numerous peptides and proteins, such as GDNF, have been characterized in recent years that they have the functions of protecting and preventing the neuronal cells from death and degeneration in vitro and in vivo, but they still cannot be used in clinic as a therapy, since they can not get through the blood brain barriers (BBB). Recently a lot of studies have shown that the human immunodeficiency virus type 1 (HIV-1) Tat protein transduction domain (PTD), is responsible for highly efficient protein transduction through the plasma membrane. In the present study, we...
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