Skin aging is driven by a combination of internal and external mechanisms, with ultraviolet (UV) radiation being a prominent external factor contributing to photoaging. Photoaging manifests through several signs, including decreased skin hydration, diminished elasticity, coarse wrinkles, and dyspigmentation. Cacao beans, known for their flavonoids and polyphenols, offer potential anti-aging benefits. To explore this, we conducted a study using both in vitro experiments and clinical trials. Our results demonstrated that cacao powder significantly improved skin hydration and moisture retention in both experimental settings. Specifically, in UVB-damaged human dermal fibroblasts (HDFs) and H₂O₂-treated keratinocytes (KCs), cacao powder displayed notable antioxidant properties. Furthermore, cacao powder enhanced the activity of antioxidant enzymes and promoted the production of hyaluronic acid in KCs, contributing to better skin hydration. It also effectively inhibited the expression of matrix metalloproteinase-1, an enzyme associated with wrinkle formation, and stimulated collagen synthesis in HDFs. Clinical trials conducted on participants with aged skin revealed a significant improvement in skin hydration and a reduction in skin wrinkles after 12 weeks of cacao powder consumption, supporting the in vitro findings. These results suggest that cacao powder holds promise as a natural ingredient for improving skin hydration and reducing wrinkles, underscoring its potential in anti-aging skincare.

Aging-associated facial hyperpigmentation is driven not only by enhanced melanogenesis but also by dermal senescence and deterioration of the dermal–epidermal junction. The purpose of this study was to evaluate whether monopolar radiofrequency (MRF) monotherapy can improve aging-related facial hyperpigmentation by simultaneously suppressing melanogenic signaling and restoring senescence-associated dermal alterations. We assumed that deep dermal heating induced by MRF would modulate fibroblast senescence and basement membrane integrity, thereby indirectly regulating melanocyte activity. In a retrospective review of 26 Asian women, MRF treatment significantly decreased multiple pigmentation parameters, including melanin level, hyperconcentration, and Hemi Melasma Area and Severity Index (hemi-MASI) scores, while concurrently reducing wrinkles, pores, and enhanced overall skin texture without inducing inflammation. Complementary ex vivo experiments using ultraviolet B (UVB)-irradiated human skin demonstrated that MRF markedly reduced pro-melanogenic markers (α-MSH, MC1R, MITF, TYR, TRP1/2), restored collagen type IV expression at the basement membrane, decreased senescence-associated genes (p16, p21), and upregulated protective heat shock proteins (HSP70/47). Together, these findings suggest that MRF improves aging-associated hyperpigmentation by both suppressing melanogenesis and rejuvenating the senescent dermal microenvironment. MRF may serve as an effective non-invasive treatment option for pigmentation disorders in aging skin.

Cutaneous fibrosis is characterized by aberrant wound healing with excessive extracellular matrix deposition, sustained inflammation, and oxidative stress, while currently available therapies show limited efficacy and safety. A Dual Hyaluronic Acid Compound (DHC), consisting of high-molecular-weight, low-molecular-weight, and minimally cross-linked hyaluronic acid, has demonstrated regenerative and antioxidant properties, but its anti-fibrotic effects have not been fully explored. This study investigated the anti-fibrotic potential of DHC using a bleomycin-induced murine dermal fibrosis model and a UVB-irradiated ex vivo human skin model. In C57BL/6 mice, dermal fibrosis was induced by daily bleomycin injections for three weeks, followed by intradermal DHC administration. Histological and biomechanical analyses showed that DHC significantly reduced dermal thickness, collagen deposition, and skin hardness compared with untreated fibrotic controls. DHC decreased α-SMA expression and increased MMP1 levels, indicating attenuation of myofibroblast activation and enhanced matrix remodeling. It also reduced macrophage markers (CD68, CD163) and pro-inflammatory cytokines (IL-1β, TNF-α). Furthermore, DHC restored superoxide dismutase (SOD) and catalase (CAT) activity and upregulated NRF2, HO-1, and NQO1 expression in the in vivo model. Similarly, DHC upregulated SOD and CAT activity and reduced pro-inflammatory cytokines (IL-6, TNF-α) in the ex vivo human skin model. These findings suggest that DHC exerts multimodal anti-fibrotic effects through coordinated regulation of fibroblast activation, inflammation, and oxidative stress, supporting its potential as a therapeutic approach for cutaneous fibrosis.

Skin aging arises from extracellular matrix degradation, inflammation, and pigmentation dysregulation, yet most existing rejuvenation strategies target only a subset of these processes. This study investigated the multimodal rejuvenation potential of a dual hyaluronic acid compound (DHC), composed of low- and high-molecular-weight HA integrated within a minimally cross-linked hybrid complex. In vitro assays using dermal fibroblasts, melanoma cells, and macrophages demonstrated that DHC enhanced fibroblast viability, collagen I/III and elastin production, antioxidant enzyme activity, and wound-healing capacity while reducing senescence markers. DHC markedly suppressed melanogenesis by downregulating the gene expression of MITF, TYR, and TRP1, and exerted strong anti-inflammatory activity by decreasing nitric oxide (NO) production and key cytokines, including TNF-α, IL-1β, IL-6, and CCL1. In a UVB-induced photoaging rat model, DHC reduced wrinkle depth, epidermal thickening, and melanin accumulation while improving elasticity, collagen density, hydration, and barrier integrity. Across these outcomes, DHC demonstrated biological effects that were comparable to, and in selected endpoints greater than, those of commonly used biostimulators and HA fillers in preclinical models. Collectively, these laboratory findings suggest that DHC exhibits broad preclinical bioactivity through combined biostimulatory, antioxidant, anti-inflammatory, and pigmentation-modulating effects. Further mechanistic and clinical studies are required to determine its translational relevance.

Plasma, an ionized gas composed of charged particles, has shown therapeutic potential in enhancing biological processes such as wound healing and tissue integration. Implants, such as silicone and human acellular dermal matrix (hADM), are commonly used in reconstructive surgery, but improving their biocompatibility and integration remains a challenge. This study investigated the effects of vacuum plasma treatment on silicone and hADM implants using an in vivo rat model. Plasma-treated and untreated implants were inserted subcutaneously, and tissue samples were collected at 1, 4, and 8 weeks post-implantation. Histological and immunohistochemical analyses were performed to assess inflammation, cellular infiltration, collagen formation (neocollagenesis), and angiogenesis. Results showed that plasma-treated silicone and hADM implants had significantly reduced capsule thickness at weeks 4 and 8 compared to untreated controls, indicating a lower chronic inflammatory response. Plasma treatment also promoted greater fibroblast infiltration and enhanced neocollagenesis within the hADM implants. Furthermore, immunohistochemical staining revealed a notable increase in blood vessel formation around and within the plasma-treated hADM implants, suggesting improved vascularization. In conclusion, vacuum plasma treatment enhances the biocompatibility and tissue integration of implants by reducing inflammation and promoting cellular and vascular responses, offering promising potential for improving outcomes in reconstructive surgery.

Injectable skin boosters currently in use mainly provide short-lived volumization or depend on inflammation-mediated collagen stimulation, raising concerns regarding durability and safety. Injectable particulate human acellular dermal matrix (phADM) is a biologically derived extracellular matrix scaffold designed to support constructive dermis remodeling. This randomized, split-face, double-blinded clinical trial evaluated the efficacy of phADM as a facial skin booster in 20 adults with moderate cheek roughness. phADM was injected on one facial side, with hyaluronic acid serving as the contralateral control. Multiple skin parameters were assessed over 20 weeks using validated imaging and biophysical instruments. Mechanistic validation was conducted using complementary in vitro, ex vivo human skin, and in vivo rat models. Clinically, the phADM-treated side demonstrated greater improvements in skin density, volume, elasticity, wrinkle depth, pore area, hydration, and barrier-related parameters at multiple time points compared with HA. In ex vivo human skin, phADM showed homogeneous dermal distribution and preservation of extracellular matrix architecture, along with restoration of basement membrane-associated proteins following UVB irradiation. In vivo rat studies revealed fibroblast infiltration and localized neocollagenesis within the implanted matrix. In vitro assays further indicated enhanced fibroblast proliferation and extracellular matrix synthesis, increased hyaluronan production, suppression of pro-inflammatory cytokines in activated macrophages, and downregulation of melanogenesis-related genes in melanoma cells. No serious adverse events were observed during the clinical study. These findings indicate that phADM functions as a restorative skin booster that promotes durable dermis remodeling and functional rejuvenation with a favorable safety profile.