AP Collagen Peptides Prevent Cortisol-Induced Decrease of Collagen Type I in Human Dermal Fibroblasts.

Area of Science:

• Biochemistry
• Dermatology
• Molecular Biology

Background:

• Cortisol, a primary stress hormone, has adverse effects on skin.
• The precise mechanisms of cortisol's impact on skin signaling are not fully understood.

Purpose of the Study:

• Investigate cortisol's effect on collagen type I expression in human dermal fibroblasts (HDFs).
• Evaluate AP collagen peptides' ability to counteract cortisol-induced inhibition of collagen type I and related signaling pathways.

Main Methods:

• Assessed cortisol's impact on collagen type I expression in HDFs.
• Utilized AP collagen peptides and glucocorticoid receptor (GR) inhibitors to study their effects.
• Examined the modulation of transforming growth factor (TGF)-β signaling.

Main Results:

• Cortisol was found to downregulate collagen type I expression.
• AP collagen peptides and GR inhibitors restored collagen type I levels and blocked GR activation.
• These agents also prevented cortisol-dependent inhibition of TGF-β signaling.
• Effectiveness was demonstrated in senescent HDFs and human skin models.

Conclusions:

• Glucocorticoid receptor (GR) signaling mediates cortisol's inhibition of TGF-β.
• AP collagen peptides function as GR-mediated signaling blockers.
• AP collagen peptides show potential for improving skin health by preventing collagen degradation.