ABSTRACT
BACKGROUND: A woman's skin is dramatically affected by pregnancy. Its biomechanical properties are critical for resisting highly stressed areas. The aim of this work was to evaluate the impact of pregnancy on the mechanical properties of skin, as well as to evaluate the imprint that pregnancy leaves on the skin after delivery. MATERIALS AND METHODS: Suction tests using a cutometer were performed on 15 non-pregnant women and 26 pregnant women at 8 months of pregnancy and 4 months after delivery. Areas of abdomen and thighs were studied. RESULTS: Significant differences between the non-pregnant and 8-month pregnant groups were observed. Our data demonstrate that skin becomes less elastic and less deformable on the abdomen during pregnancy. On the thighs, a loss of elasticity and firmness was also observed. At 4 months after delivery, the skin did not return to its initial state. CONCLUSION: This study showed that the mechanical properties of skin changed drastically during pregnancy compared to the non-pregnant condition and that these properties remain altered 4 months after delivery. In addition to alterations in abdominal skin during pregnancy, we also observed mechanical changes on the thighs, which are less subject to stretching.
Subject(s)
Pregnancy/physiology , Skin Physiological Phenomena , Abdomen/physiology , Adult , Biomechanical Phenomena , Female , Humans , Thigh/physiology , Young AdultABSTRACT
The antiaging efficacy of retinol (ROL) has been explored mainly clinically in photoprotected skin sites and for high doses of ROL (0.4-1.6%). The objective of the study was to demonstrate the antiaging action of a low and tolerable dose of ROL (0.1%) ex vivo by measuring the expression of cellular retinoic-acid-binding protein II (CRABP2) and heparin-binding epidermal growth factor (HBEGF) by a histological evaluation of the epidermis and in vivo by assessing major aging signs and performing three-dimensional profilometry and digital imaging during a 9-month double-blind placebo-controlled study involving 48 volunteers. Finally, epidermal cell proliferation was evaluated using tryptophan fluorescence spectroscopy. Our results demonstrate that 0.1% ROL induced CRABP2 and HBEGF gene expression and increased keratinocyte proliferation and epidermal thickness. In human volunteers, topical application of a ROL-containing product improved all major aging signs assessed in our study (wrinkles under the eyes, fine lines and tone evenness). Moreover, tryptophan fluorescence increased in the active-agent-treated group and not in the placebo-treated group, indicating that cell proliferation was accelerated in vivo. These data demonstrate that a product containing a low dose (0.1%) of ROL promotes keratinocyte proliferation ex vivo and in vivo, induces epidermal thickening ex vivo and alleviates skin aging signs, without any significant adverse reaction.
Subject(s)
Gene Expression Regulation/drug effects , Skin Aging/drug effects , Vitamin A/pharmacology , Vitamins/pharmacology , Administration, Cutaneous , Adult , Cell Proliferation/drug effects , Double-Blind Method , Epidermal Cells , Epidermis/drug effects , Female , Heparin-binding EGF-like Growth Factor , Humans , Intercellular Signaling Peptides and Proteins/genetics , Keratinocytes/drug effects , Keratinocytes/metabolism , Middle Aged , Receptors, Retinoic Acid/genetics , Skin Aging/genetics , Spectrometry, Fluorescence , Tryptophan/chemistry , Vitamin A/administration & dosage , Vitamin A/adverse effects , Vitamins/administration & dosage , Vitamins/adverse effectsABSTRACT
Compound S 17092 is a potent and selective inhibitor of prolyl endopeptidase (EC 3.4.21.26, PEP) that may be of therapeutic value for the treatment of memory impairment associated with neurodegenerative diseases. In the present study, we investigated the effects of S 17092 on the catabolism of the promnesic neuropeptides thyrotrophin-releasing hormone (TRH) and arginine-vasopressin (AVP) in the rat brain. In vitro, bacterial PEP hydrolysed both TRH and AVP, and the breakdown of the two peptides was almost completely prevented by 10(-5) M S 17092. In vivo, a single oral administration of S 17092 provoked a significant increase in TRH-like immunoreactivity (TRH-LI) in the cerebral cortex (+63% for a 10 mg/kg dose and +72% for a 30 mg/kg dose), as well as AVP-LI in the hippocampus (+54% for a 30 mg/kg dose), but did not affect TRH-LI in the amygdala nor AVP-LI in the cerebral cortex. Chronic administration of S 17092 (10 or 30 mg/kg daily) lead to a significant increase in THR-LI in the cerebral cortex (+55% and +56%, respectively), but did not modify AVP-LI in the hippocampus, nor in the cerebral cortex. These results show that the selective PEP inhibitor S 17092 increases TRH and AVP content in discrete regions of the rat brain. The present data suggest that the promnesic and antiamnesic effects of S 17092 can be accounted for, at least in part, by blockage of AVP and TRH degradation by PEP.
