CN-121987530-A - Method for regulating synthesis of fibroblast and degrading hyaluronic acid

Abstract

The invention relates to a novel method for regulating synthesis and degradation of hyaluronic acid by fibroblasts, which is characterized by comprising the use of at least one selected from nerol, carvacrol, geraniol, agilawood essential oil and sandalwood essential oil.

Inventors

• LI TAN
• LI JUEQIAN

Assignees

• 株式会社资生堂

Dates

Publication Date

20260508

Application Date

20241101

Claims (6)

1. 1. A method for regulating fibroblast synthesis and degrading hyaluronic acid, comprising using at least one selected from the group consisting of nerol, carvacrol, geraniol, agilawood essential oil, and sandalwood essential oil.
2. 2. The method of claim 1, comprising using at least one of a hyaluronic acid synthase (HAS 2) expression promoter comprising at least one selected from the group consisting of nerol, carvacrol, and geraniol or a hyaluronic acid degrading enzyme (HYBID) expression inhibitor comprising at least one selected from the group consisting of nerol, carvacrol, an agilawood essential oil, and a santalum essential oil.
3. 3. A method for preventing skin aging comprises applying to skin a cosmetic containing at least one selected from nerol, carvacrol, geraniol, lignum Aquilariae Resinatum essential oil, and lignum Santali albi essential oil.
4. 4. Use of at least one of nerol, carvacrol, geraniol, agilawood essential oil, sandalwood essential oil for preparing a cosmetic with anti-aging effect.
5. 5. Use of nerol, carvacrol or geraniol for the preparation of a hyaluronic acid synthase expression promoter.
6. 6. Use of nerol, carvacrol, agilawood essential oil or santalum album essential oil for the preparation of an inhibitor of expression of hyaluronic acid degrading enzymes.

Description

Method for regulating synthesis of fibroblast and degrading hyaluronic acid Technical Field The present invention relates to a method for regulating fibroblast synthesis and degrading hyaluronic acid, and a method for resisting skin aging. Background Skin aging is a result of the combined effects of natural aging and photoaging of the skin, and is manifested by reduced skin elasticity, increased wrinkles, stain formation, and the like. Fibroblasts (fibroblastic), also known as fibroblasts, are the major cellular component of loose connective tissue, differentiated from mesenchymal cells in embryonic stages. Such cells account for over 95% of all cells in the dermis. It can be said that the maintenance of the structure and function of the whole dermis layer is maintained by the main force of the fibroblast, thereby well maintaining the firmness, elasticity and moisture of the skin. Hyaluronic Acid (HA) is an important biological macromolecule present in the skin and HAs various biological functions of keeping the skin moist, promoting cell proliferation and migration, regulating inflammatory reaction, etc. The synthesis and degradation process of hyaluronic acid is affected by a number of factors, of which the hyaluronic acid synthase (HA SYNTHETASE, HAS) and the hyaluronic acid degrading enzyme (hyaluronan binding protein involved in hyaluronan depolymerization, HYBID) play a key role. Mammals have 3 HAS subtypes, HA synthase 1 (HAS 1), HA synthase 2 (HAS 2), and HA synthase 3 (HAS 3). Degradation of HA in human dermal tissue is mediated primarily by HYBID. Increased expression of HYBID and decreased expression of HAS1 and HAS2 was detected in photo-aged skin samples, indicating that an imbalance between HYBID-mediated HA degradation and HAS-mediated HA synthesis may lead to an increase in HA catabolism in photo-aged skin, a decrease in HA in the dermal papilla layer, and ultimately skin wrinkles and sagging. It has been reported that the production of hyaluronic acid from dermal fibroblasts is as high as 12-60 pg/cell/24 h, about 10 times the production of hyaluronic acid from keratinocytes. The synthesis of hyaluronic acid in normal human skin fibroblasts is mainly responsible for HAS1 and HAS2, with HAS2 being the major HAS subtype expressed in fibroblasts. Overall, the amount of hyaluronic acid synthesized was consistent with the mRNA expression level of HAS 2. Growth factors such as TGF-. Beta.1, PDGF-BB, EGF and bFGF can all increase the synthetic yield of hyaluronic acid by upregulating HAS in normal human skin fibroblasts. TGF-beta differentially regulates expression of HAS subtypes in fibroblasts and keratinocytes, TGF-beta upregulates expression of HAS1 and HAS2 in fibroblasts, TGF-beta induces HAS1 expression only in keratinocytes, HAS no effect on HAS2, suggesting that dermal and epidermal hyaluronic acid are independently regulated. Studies at the cellular level have found that cellular senescence is closely related to decreased synthesis of HA. Both senescent and aged fibroblasts had significantly reduced capacity to synthesize HA compared to young and non-senescent fibroblasts, and had significantly reduced expression levels of HAs 2. By comparing the ability of fibroblasts isolated from human skin samples of different ages to express HAS, hyaluronidase and secrete HA, it was found that the elderly fibroblasts secrete less HA, and that HAS, and in particular HAS2, is down-regulated without significant changes in hyaluronidase expression, further suggesting that the lack of HA in the aged dermis may be due to insufficient HA secretion by the elderly fibroblasts, and that the decrease in the ability to secrete HA is primarily related to down-regulation of HAS2 expression but not to the expression level of hyaluronidase. The exogenous HA is supplemented, so that the external HA HAs certain curative effects of improving the appearance of skin and resisting skin aging. The exogenous supplementary HA can make up for the deficiency of endogenous HA of aging skin, HAs the functions of moisturizing, physically filling and the like, also HAs the biological effects of strengthening skin barrier, promoting repair, stimulating regeneration, inducing collagen, resisting oxidative stress and the like, HAs been proved by a large number of researches to have the skin aging effect and is widely applied. However, the macromolecular HA is poorly absorbed transdermally when applied externally, and the exogenous HA is rapidly cleared in skin tissues, which greatly limits the exertion of the skin care efficacy of the exogenous HA. Thus, modulation of endogenous HA levels in the skin constitutes a unique skin delay strategy. There are two possible strategies for directly modulating the HA level of skin by topical application of small molecule compounds or plant extracts, either by promoting HA synthesis or by down-regulating HA degrading enzymes. Increasing the mRNA expression level of HAS or increasing the HA yield