Abstract
Thymosin β4 (Tβ4) is a multifunctional and widely distributed peptide that plays a pivotal role in several physiological and pathological processes in the body, namely, increasing angiogenesis and proliferation and inhibiting apoptosis and inflammation. Moreover, Tβ4 is effectively utilized for several indications in animal experiments or clinical trials, such as myocardial infarction and myocardial ischemia-reperfusion injury, xerophthalmia, liver and renal fibrosis, ulcerative colitis and colon cancer, and skin trauma. Recent studies have reported the potential application of Tβ4 and its underlying mechanisms. The present study reveals the progress regarding functions and applications of Tβ4.
Highlights
Thymosin is a lymphocyte growth factor that was initially extracted from the calf thymus by Goldstein and White [1]
Chen et al reported that Thymosin b4 (Tb4) reduced the expression of transforming growth factor (TGF)- b1, TGFbR II, Smad2, and Smad3 in the liver tissues of mice with bile duct ligation. They demonstrated that Tb4 reduced TGFbR II expression level in human hepatic stellate cells LX-2 in vitro. These results indicated that Tb4 alleviated cholestatic liver fibrosis by inhibiting the TGFb/Smad pathway [51]
A randomized double-blind clinical phase II trial revealed that the Tb4 treatment group revealed a 35.1% reduction in ocular discomfort than that of the vehicle control group and a 59.1% reduction in total corneal fluorescein staining than that of the vehicle control group
Summary
Thymosin is a lymphocyte growth factor that was initially extracted from the calf thymus by Goldstein and White [1]. Tb4 can promote cell migration and angiogenesis, regulate various cytokines, such as intercellular adhesion molecule (ICAM-1), MMP, laminin (LN), VEGF, and basic fibroblast growth factor, inhibit apoptosis, eliminate inflammation, and reduce oxidative damage [91, 92] It can increase cell migration in various injury models, the migration of keratinocytes, which cover the wound and protect from fluid loss and infection [81, 93,94,95,96]. In a full-thickness skin defect Sprague-Dawley rats rat model, VEGF and basic fibroblast growth factor revealed sustained and stable high expression after treatment with recombinant Tb4, which inhibited LN-5 expression in the early stage, beneficial for cell proliferation and differentiation; it upregulated LN-5 expression in the middle and late stages, which was beneficial for improving the matrix environment and promoting epidermal cell migration and wound healing [98].
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