Thymosin β4 as a multifunctional bioactive molecule plays a key role in the protection of nerve tissue and in the treatment of traumatic and neurological brain damage. In the quoted article, the authors pay attention to the protective effect of Tβ4 in 4 cases: neuronal damage, glial cell injury, defense of nervous tissue through anti-inflammatory effects and regeneration of cerebral vessels.

Tβ4 plays a key role in many cellular processes including mobility, neurite formation, proliferation, and neuronal survival. Treatment with exogenous Tβ4 increases the survival of neurons after spinal cord injury in rats, the number of surviving neurons and oligodendrocytes in animals treated with Tβ4 increased significantly.

Moreover, in an animal model of traumatic brain injury, early treatment with intraperitoneal injection of Tβ4 reduces cortical volume and hippocampal cell loss and improves functional recovery, indicating that a neuroprotective effect is possible. The substance also significantly reduces apoptosis of neuronal progenitor cells caused by a reduction in the supply of oxyglucose.

Glial cells are the interstitial cells of the nervous system. They support and nourish neurons. They also participate in transduction and information transmission in the brain, regulate the secretion and uptake of neurotransmitters, and maintain environmental balance in the brain. Glial cells are mainly astrocytes, oligodendrocytes and microglia.

Tβ4 may reduce the neurotoxicity of ethanol to astrocytes and has a significant protective effect, suggesting that Tβ4 may protect astrocytes and reduce their damage by inhibiting apoptosis.

Tβ4 promotes oligodendrocyte differentiation and inhibition of the Toll-like receptor pro-inflammatory pathway, suggesting that Tβ4 has development prospects in the treatment of nerve damage. Tβ4 by inhibiting nuclear factor kB activation to protect oligodendrocytes from damage and death appears to be a way to treat demyelinating diseases.

Also described is the use of Tβ4 to treat microglial cells in mice with hypoxic brain injury, and it was found that Tβ4 can inhibit inflammatory mediators such as TNF-α and interleukin-1β secretion, and may be involved in microglia activation after chronic cerebral ischemia, which promotes recovery. nervous functions.

Tβ4 has been used to treat a variety of neurological diseases. Increasing evidence suggests that the effects of thymosin have anti-inflammatory potential in a variety of inflammation and autoimmune diseases. For example, treatment with Tβ4 may improve recovery from experimental autoimmune encephalomyelitis by reducing the inflammatory infiltration and stimulating the production of oligodendrocytes.

The mechanism of Tβ4 promoting angiogenesis is still under extensive research, and the most important elements are: The combination of Tβ4 and G-actin increases endothelial cell proliferation and adhesion, and promotes endothelial cell migration. Induction of increased secretion of pro-angiogenic factors such as vascular endothelial growth factor and matrix metalloproteinases. Activating pro-angiogenic pathways such as the phosphoinositide 3-kinase / protein kinase B pathway.

The entire article is available at:

https://doi.org/10.1177%2F2058739220934559