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Thymosin-alpha-1

Thymalfasin, Zadaxin, Thymosin α1

Quick Stats
Studies 759
Trials 63
Score 2
1983 pubmed

Thymosin peptides and lymphokines do not directly stimulate adrenal corticosteroid production in vitro.

Vahouny. G V GV; Kyeyune-Nyombi. E E; McGillis. J P JP; Tare. N S NS; Huang. K Y KY; Tombes. R R; Goldstein. A L AL; Hall. N R NR

Key Findings

  • Thymosin-alpha-1, alpha-7, and beta-4 did not stimulate steroid production in isolated rat adrenal fasciculata cells.
  • These peptides did not enhance the adrenal response to ACTH nor increase cAMP in adrenal membrane preparations.
  • Lymphokine-containing spleen cell supernatants and mouse interferon also failed to affect adrenal steroidogenesis directly.

Practical Outcomes

  • For biohackers, taking thymosin-alpha-1 is unlikely to directly raise cortisol or other adrenal steroids, so it shouldn't be used as a quick adrenal boost. Any hormonal effects observed in humans are probably mediated through the nervous system, meaning dosing strategies aimed at adrenal stimulation are not supported by this data.

Summary

The study found that thymosin-alpha-1 and related thymosin peptides do NOT directly cause rat adrenal cells to make more steroid hormones in a dish, and they don't boost the cells' response to ACTH. Any steroid increase seen in living animals is probably due to brain signals, not a direct adrenal effect.

Abstract

There is developing evidence that certain thymosin peptides and lymphokines produce a transient increase in steroid hormones when introduced systemically. Conversely, the repressive effect of adrenocortical steroids on the immune system is well documented. In the present study, the direct effect of certain components of the immune system on steroid output by rat adrenal fasciculata cells was tested. With this system, there was no direct steroidogenic effect of either the partially purified thymosin fraction 5, or any of the purified peptide components tested (thymosin alpha 1, alpha 7, or beta 4). These peptides also did not synergize the cellular response to ACTH, nor did they induce cAMP production by a ACTH- and NaF-responsive adrenal membrane preparation. Supernatants from Con A-stimulated spleen cells, which were demonstrated to contain lymphokine activity, and partially purified mouse interferon were also without a significant direct or synergistic effect on steroidogenesis by adrenocortical cells. These results suggest that the steroidogenic response to these peptides observed in vivo may be mediated by the central nervous system.

Study Information

Provider

pubmed

Year

1983