Xerosis, characterized by dry, rough skin, causes discomfort and aesthetic concerns, necessitating effective treatment. Traditional treatments often show limited efficacy, prompting the need for innovative therapies. This study highlights the efficacy of microbiome therapeutic LP51, derived from a healthy vaginal microbiome, in improving xerosis. A double-blind clinical trial involving 43 subjects with dry inner arm skin compared the effects of a 2.9% LP51 extract formulation to a placebo over 4 weeks. The LP51 group exhibited a significant increase in stratum corneum hydration (10.0 A.U.) compared to the placebo group (4.8 A.U.) and a 21.4% decrease in transepidermal water loss (TEWL), whereas the placebo group showed no significant change. LP51 also demonstrated benefits in enhancing skin hydration, improving the skin barrier, and exhibited anti-atopic, anti-inflammatory, and antioxidant properties. Safety was confirmed through in vitro cytotoxicity tests. These effects are attributed to the microbiome-safe component in LP51 and its role in improving xerosis, reflected by an increase in the xerosis-microbiome index, defined by the Firmicutes/Actinobacteria ratio. These findings position microbiome therapeutic LP51 as a promising novel treatment for xerosis.

The sebum on human skin is generated for various causes. The composition of the formed sebum increases the proliferation of Cutibacterium acnes (C. acnes) residing on the skin. As C. acnes proliferates, it produces skin irritants that stimulate the sebaceous glands, increasing sebum production. Skin troubles such as acne may occur. The lysate concentrates of Bacillus stratosphericus (B. stratosphericus), first discovered in the stratosphere, confirmed a 66.35% inhibition of Nitric Oxide (NO) production at 0.50 mg/ml concentration in vitro. Additionally, the growth inhibition efficacy of B. stratosphericus lysate concentrate (BSLC) against C. acnes was confirmed, showing a 95.1% inhibition of growth proliferation at a consistency of 0.50 mg/ml. Based on the in vitro results, the efficacy of BSLC in degrading and reducing sebum was confirmed by reacting it with artificial sebum to various concentrations. The results showed a concentration-dependent decrease in artificial sebum ccording to the efficacy results confirmed in vitro, a clinical trial was conducted to evaluate the daily sebum reduction efficacy of a serum formulation containing 50 mg/ml of BSLC. After a 4-week application, the test group containing BSLC determined a significant 28.68% reduction in sebum levels, demonstrating the practical implications of the research. In conclusion, BSLC is considered to have sufficient industrial value as a valuable ingredient for the cosmetics industry aimed at sebum improvement.

Skin photoaging is largely driven by ultraviolet (UV) irradiation, which contributes to chronic inflammation and extracellular matrix (ECM) degradation. This study investigated the protective effects of paeonol against UVB-induced cellular senescence in human dermal fibroblasts (HDFn). Repeated UVB irradiation was used to induce premature senescence. Paeonol treatment reduced the senescence-associated β-galactosidase (SA-β-gal) positive cells and intracellular reactive oxygen species (ROS) accumulation. Paeonol also reduced the expression of senescence-associated cell cycle regulators, including p21 and p16 at the mRNA level and the protein level. In addition, paeonol suppressed matrix metalloproteinase-1 (MMP-1) production but did not significantly restore type I procollagen secretion. Paeonol also attenuated the expression and secretion of the senescence-associated secretory phenotype (SASP) factors inter-leukin-6 (IL-6) and interleukin-8 (IL-8). These effects were accompanied by reduced phosphorylation of JNK and c-Jun. Furthermore, activation of JNK signaling with anisomycin partially reversed the paeonol-mediated suppression of MMP-1 mRNA expression, supporting the involvement of JNK signaling in the regulation of MMP-1. Collectively, these findings suggest that paeonol attenuates multiple features of UVB-induced cellular senescence in HDFn cells, with JNK signaling potentially contributing to its inhibitory effect on MMP-1 expression. Further studies are needed to clarify the mechanisms underlying these effects and establish their physiological relevance in UVA-based and in vivo models.