We have evaluated the efficacy of early Tβ4 treatment on spatial learning and sensorimotor functional recovery in rats after TBI induced by unilateral CCI.34 In brief, TBI rats received Tβ4 at a dose of either 6 or 30 mg/kg (RegeneRx Biopharmaceuticals Inc, Rockville, MD) or a vehicle control (saline) administered i.p. starting at 6 hours after injury and then at 24 and 48 hours. Spatial learning was performed during the last five days (31-35 days post injury) using the modified Morris water maze (MWM) test, which is extremely sensitive to the hippocampal injury.35-37 Tβ4-treated TBI rats showed significant improvement in spatial learning when compared to the saline-treated TBI rats. Tβ4 treatment also significantly reduced the swim latency to reach the hidden platform by rats post TBI compared to saline treatment. Using the modified Neurological Severity Score (mNSS) test, our data show that significantly improved scores were observed after TBI in the Tβ4-treated group compared to the saline-treated group. Our data also show that Tβ4 reduced the incidence of both right forelimb and hindlimb footfaults in TBI rats.34 Histological data show that early Tβ4 treatment reduced cortical lesion volume by 20% and 30% for 6 mg/kg and 30 mg/kg, respectively, and reduced hippocampal cell loss. These findings suggest that TB4 provides neuroprotection even when the treatment was initiated 6 hours post injury. In addition, 6-hour Tβ4 treatment promotes neurogenesis in the dentate gyrus (DG) of the hippocampus,38 which may contribute to improvement in spatial learning.
Thymosin Beta 4 is a potent peptide that comes from a family of 16 related molecules that are localized in circulating cells and tissues within the body. These molecules also have a high conservation of sequence. TB 500 conjoins with actin and prevents actin polymerization. It is noted as being the actin-sequestering molecule within eukaryotic cells. It also boosts extracellular matrix-degrading enzyme production.
Skin is the largest organ of the body, which makes up 16% of total body weight. It is also the largest organ that provides immune protection and plays a role in inflammation. Composed of specialized epithelial and connective tissue cells, skin is our major interface with the environment, a shield from the outside world and a means of interacting with it. As such, the skin is subjected to insults and injuries: burns from the sun’s ultraviolet radiation that elicit inflammatory reactions, damage from environmental pollutants and wear and tear that comes with aging.
The oxytocin peptide is synthesized as an inactive precursor protein from the OXT gene. This precursor protein also includes the oxytocin carrier protein neurophysin I. The inactive precursor protein is progressively hydrolyzed into smaller fragments (one of which is neurophysin I) via a series of enzymes. The last hydrolysis that releases the active oxytocin nonapeptide is catalyzed by peptidylglycine alpha-amidating monooxygenase (PAM).
Potential side effects of 5-HTP include heartburn, stomach pain, nausea, vomiting, diarrhea, drowsiness, sexual problems, vivid dreams or nightmares, and muscle problems. Because 5-HTP has not been thoroughly studied in a clinical setting, possible side effects and interactions with other drugs are not well known. According to the US National Institute of Health TOXNET, 5-HTP has not been associated with serotonin syndrome or any serious adverse events in humans. Across multiple studies, 5-HTP also been reported to not cause any noticeable hematological or cardiovascular changes. 5-HTP also has not been associated with eosinophilia.