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Home / Research / How can Thymosin Beta4 (TB500) improve recovery, inflammation, neuropathies, fibrosis, telomerase and senescent cell removal?
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How can Thymosin Beta4 (TB500) improve recovery, inflammation, neuropathies, fibrosis, telomerase and senescent cell removal?

Descriptive of the published preclinical literature, for research and educational purposes only — not therapeutic claims about any ai-peptides product.

Thymosin B4 Reduces Inflammation by Upregulating MicroRNA-146a and Promotes Myelin

“Tissue inflammation results from neurological injury, and regulation of the inflammatory response is vital for neurological recovery. The innate immune response system, which includes the Toll-like receptor (TLR) proinflammatory signaling pathway, regulates tissue injury… TB4-mediated oligodendrogenesis results from [up-regulating] miR-146a [causing the] suppression [of] the TLR proinflammatory pathway and modulation of the p38 MAPK pathway.” (8)“By targeting IRAK1 and TRAF6, miR-146 inhibits NF-κB activation. We therefore hypothesized that TB4 regulates the TLR proinflammatory signaling pathway by specifically regulating miR-146a to promote differentiation of OPCs [oligodendrocyte progenitor cells] to mature myelin basic protein (MBP)-expressing OLs [oligodendrocytes]… transfection with anti-miR-146a inhibitor nucleotides significantly inhibited the expression of MBP and phosphorylation of p38 MAPK.” (8)

For laboratory and scientific research use only. Not for human or veterinary use. Statements have not been evaluated by the US Food and Drug Administration.

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