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Thymosin-alpha-1

Thymalfasin, Zadaxin, Thymosin α1

Quick Stats
Studies 759
Trials 63
Score 2
1992 pubmed 18 citations

Effect of thymosin alpha 1 on hypothalamic hormone release.

Milenkovic. L L; Lyson. K K; Aguila. M C MC; McCann. S M SM

Key Findings

  • Thymosin‑alpha‑1 inhibits TRH release from hypothalamic fragments at a minimal effective dose of 10⁻ÂčÂč M
  • It also suppresses CRH and somatostatin release, but requires a higher dose of 10⁻âč M
  • The peptide’s potency follows TRH > CRH > somatostatin, matching earlier in‑vivo findings on pituitary hormone drops

Practical Outcomes

  • Tα1 might be able to blunt thyroid‑stimulating and stress‑related hormone cascades, which could be attractive for those seeking to lower TSH or cortisol. Yet, because the data are from an in‑vitro mouse model, there’s no clear guidance on safe or effective human dosing, so it’s not ready for protocol changes without further research.

Summary

The study shows that the peptide thymosin‑alpha‑1 can directly suppress the brain’s release of hormones that control the thyroid (TRH), stress (CRH) and growth hormone regulation (somatostatin) in a lab dish, and it does this at very tiny concentrations. However, the work was done on isolated mouse hypothalamus tissue, not in people, so we don’t know how it translates to real‑world dosing or effects.

Abstract

Thymosin alpha 1 (T alpha 1) is a well-characterized immunopotentiating polypeptide originally isolated from calf thymus. We have recently shown in vivo, probable hypothalamic effects of T alpha 1 to decrease the release of the pituitary hormones, TSH, PRL and ACTH from the pituitary gland. Therefore, in the present study we evaluated the effect of the peptide on the release of hypothalamic regulatory hormones: thyrotropin-releasing hormone (TRH) and corticotropin-releasing hormone (CRH), as well as somatostatin (SRIH), from medial basal hypothalamic (MBH) fragments incubated in vitro. After a preliminary time-course study indicated that a 30-min incubation period was optimal, it was used for all the other experiments. At the end of the incubation the tissue was still able to respond to a depolarizing K+ concentration for 15 min by a 4-fold increase of TRH concentration compared to control basal release during the preceding 30 min. T alpha 1 was shown to inhibit the release of TRH and CRH from MBH fragments incubated in vitro with a minimal effective dose (MED) of 10(-11) M. SRIH and CRH release was also inhibited but the MED for these peptides was 10(-9) M. The relative responsiveness to the action of T alpha 1 was TRH greater than CRH, which was greater than SRIH. This correlated with our previous in vivo results for pituitary hormone release, except in the case of SRIH since we previously did not detect any significant effect of the peptide on growth hormone release. Finally, we evaluated the possible involvement of other neurotransmitters in the effect of T alpha 1 on TRH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Study Information

Provider

pubmed

Year

1992

Date

1992-07-01T00:00:00.000Z

DOI

10.1159/000126292

Citations

18