Neuroprotective and neurorestorative effects of thymosin ?4 treatment following experimental traumatic brain injury
Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. No effective pharmacological treatments are available for TBI because all phase II/III TBI clinical trials have failed. This highlights a compelling need to develop effective treatments for TBI. Endogenous neurorestoration occurs in the brain after TBI, including angiogenesis, neurogenesis, synaptogenesis, oligodendrogenesis, and axonal remodeling, which may be associated with spontaneous functional recovery after TBI. However, the endogenous neurorestoration following TBI is limited. Treatments amplifying these neurorestorative processes may promote functional recovery after TBI. Thymosin beta 4 (T?4) is the major G-actinsequestering molecule in eukaryotic cells. In addition, T?4 has other properties including antiapoptosis and anti-inflammation, promotion of angiogenesis, wound healing, stem/progenitor cell differentiation, and cell migration and survival, which provide the scientific foundation for the corneal, dermal, and cardiac wound repair multicenter clinical trials. Here, we describe T?4 as a neuroprotective and neurorestorative candidate for treatment of TBI.
neuroprotection neurorestoration traumatic brain injury thymosin beta 4 rat