TB-500 and the Nervous System
Studies suggest that after the damage to the central and peripheral nerve systems, TB-500 may promote healing and remodeling in rats. The study suggests that TB-500 may stimulate the cells that support neurons; however, the specific method has yet to be understood. Oligodendrocytes are considered responsible for maintaining a healthy neuronal population [i]. A substantial laboratory outcome that is mirrored in clinically meaningful improvements in behavior, motor control, and cognitive assessments was found when their activity was increased in brain areas that had been damaged [ii].
In a recent study, TB-500 appeared to increase the survival of transplanted neural stem/progenitor cells (NSPCs) and decrease oxidative stress after spinal cord damage while improving spinal regeneration [iii].
TB-500 and Blood Vessels
Capillary (small blood vessel) expansion is considered important for several physiological processes, including wound healing and hair growth, and VEGF is a possible key signaling molecule in this process [iv]. However, TB-500 is speculated to play a more nuanced function than this. Extracellular matrix remodeling, vasculogenesis, angiogenesis, and the differentiation of more primitive mesenchymal tissue into the specialized endothelial tissue that lines blood vessels are all processes scientists hypothesize may be supported by the peptide. This hypothesis has some basis since studies have suggested that lacking TB-4 may disrupt blood vessel development and stability. At the same time, when given, it may promote capillary formation and the recruitment of pericytes after injury [iv].
TB-500 and Hair
Researchers noticed that when shaved for lab tests, the hair of TB-4-deficient mice came back considerably more slowly than that of wild-type mice. Researchers suggested that genetically engineered mice with elevated TB-4 production appeared to have much quicker hair regrowth than wild-type mice. It was suggested that microscopically, these mice appeared to have more hair shafts and clusters of hair follicles than normal [v].
TB-500 and Infection
In mice with an eye infection caused by Pseudomonas aeruginosa, researchers speculated that giving TB-4 with an antibiotic compound appeared to increase the compound’s efficacy, accelerate healing, and decrease inflammation. Colony-forming unit (CFU) counts, neutrophil (white blood cell) counts, and inflammatory reactive oxygen species (ROS) levels appeared to be reduced after just five days of combination [vi].
TB-500 and the Heart
Studies suggest the cardiovascular and renal systems may be aided by TB-4 and its derivatives, as has been speculated in research spanning two decades. However, how exactly these properties are brought about remains unclear. Multiple mechanisms have been proposed to account for the properties suggested in studies. To begin with, TB-500’s potential to stimulate the development of collateral blood vessels may induce functional restoration. Second, studies suggest TB-500 may promote the survival of myocytes and the migration of endothelial cells after a heart attack. Scientists hypothesize TB-500 may lower inflammation and fibrosis (scar development) by interacting with other natural signaling molecules [vii].
Collagen-and-TB-4 hydrogels have recently been studied for their potential to induce angiogenesis and epicardial heart cell migration, increasing recovery rates post-ischemia and decreasing scarring, minimizing long-term complications [viii].
TB-500 and Neurodegeneration
One recent research study suggested that TB-4 may improve autophagy, thereby possibly improving the immune system’s capacity to cope with prion protein [ix]. Autophagy in the brain and spinal cord is considered to protect neurons from degeneration.
More investigation is required to explore its potential in scientific research, and these studies must continue. Only academic and scientific institutions are allowed to use Thymosin Beta-4 peptides. If you are a licensed professional interested in to buy peptides for your clinical studies, visit Biotech Peptides. Please note that none of the items mentioned are approved for human or animal consumption. Laboratory research chemicals are only for in-vitro and in-lab use. Any kind of physical introduction is illegal. Only authorized academics and working professionals may make purchases. The content of this article is intended only for instructional purposes.
[i] P. Cheng, F. Kuang, H. Zhang, G. Ju, and J. Wang, “Beneficial effects of thymosin β4 on spinal cord injury in the rat,” Neuropharmacology, vol. 85, pp. 408–416, Oct. 2014. [PubMed]
[ii] M. Chopp and Z. G. Zhang, “Thymosin β4 as a restorative/regenerative therapy for neurological injury and neurodegenerative diseases,” Expert Opin. Biol. Ther., vol. 15 Suppl 1, pp. S9-12, 2015. [PubMed]
[iii] H. Li, Y. Wang, X. Hu, B. Ma, and H. Zhang, “Thymosin beta 4 attenuates oxidative stress-induced injury of spinal cord-derived neural stem/progenitor cells through the TLR4/MyD88 pathway,” Gene, vol. 707, pp. 136–142, May 2019. [PubMed]
[iv] K. N. Dubé and N. Smart, “Thymosin β4 and the vasculature: multiple roles in development, repair and protection against disease,” Expert Opin. Biol. Ther., vol. 18, no. sup1, pp. 131–139, 2018. [PubMed]
[v] D. Philp, S. St-Surin, H.-J. Cha, H.-S. Moon, H. K. Kleinman, and M. Elkin, “Thymosin beta 4 induces hair growth via stem cell migration and differentiation,” Ann. N. Y. Acad. Sci., vol. 1112, pp. 95–103, Sep. 2007. [PubMed]
[vi] T. W. Carion et al., “Thymosin Beta-4 and Ciprofloxacin Adjunctive Therapy Improves Pseudomonas aeruginosa-Induced Keratitis,” Cells, vol. 7, no. 10, Sep. 2018. [PubMed]
[vii] K. M. Kassem, S. Vaid, H. Peng, S. Sarkar, and N.-E. Rhaleb, “Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?,” Can. J. Physiol. Pharmacol., pp. 1–11, Mar. 2019. [PubMed]
[viii] A. D. Shaghiera, P. Widiyanti, and H. Yusuf, “Synthesis and Characterization of Injectable Hydrogels with Varying Collagen–Chitosan–Thymosin β4 Composition for Myocardial Infarction Therapy,” J. Funct. Biomater., vol. 9, no. 2, Mar. 2018. [PubMed]
[ix] H.-J. Han, S. Kim, and J. Kwon, “Thymosin beta 4-Induced Autophagy Increases Cholinergic Signaling in PrP (106-126)-Treated HT22 Cells,” Neurotox. Res., Dec. 2018. [PubMed]
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