Ling Ma

Psychological stress activates the local hypothalamic–pituitary–adrenal (HPA)-like axis in hair follicles, leading to cortisol overproduction and dysfunction of dermal papilla cells (DPCs). However, effective natural ingredients targeting this mechanism remain scarce. To investigate whether Camellia nitidissima flower extract (CNF) alleviates stress-induced DPC dysfunction by inhibiting 11β-Hydroxysteroid dehydrogenase type 1(11β-HSD1) and modulating the downstream signaling pathways. The phytochemical composition of CNF was characterized using HPLC-DAD. An in vitro stress-induced injury model was established in human DPCs using corticotropin-releasing factor (CRF). Cortisol levels as well as the secretion levels of hair growth factors were measured by ELISA. The expression of 11β-HSD1 was assessed via immunofluorescence. Oxidative stress was evaluated by reactive oxygen species (ROS) fluorescence and superoxide dismutase (SOD) activity. Apoptosis was analyzed by flow cytometry (Annexin V-FITC/PI). Protein expression of the TGF-β2/Smad pathway and mitochondrial apoptosis-related proteins was detected by western blotting. Cell proliferation was assessed by Ki67 immunofluorescence and cell cycle analysis. The mRNA expression of Wnt/β-catenin pathway components was quantified by Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Ten bioactive constituents, predominantly the polyphenolic compounds rutin and quercetin-7-O-β-D-glucoside, were identified in CNF. Mechanistically, CNF disrupted the local “stress-cortisol” amplification loop by first reducing CRF-induced cortisol secretion and downregulating 11β-HSD1 expression in DPCs. This upstream intervention subsequently attenuated oxidative stress and inhibited CRF-induced apoptosis via suppression of the TGF-β2/Smad2/3 pathway, while concurrently restoring proliferative capacity through reactivation of the Wnt/β-catenin signaling axis. These coordinated molecular events ultimately reinstated the secretion of key hair growth factors, including Alkaline phosphatase (ALP), Vascular endothelial growth factor (VEGF), Hepatocyte growth factor (HGF), Epidermal growth factor (EGF), and insulin-like growth factor 1 (IGF-1), thereby mitigating DPC dysfunction.

Stress-induced sebaceous hyperactivity is a key driver of acne and seborrheic dermatitis; however, research investigating the pathway-specific mechanisms through which stress exerts its effects and the suppression of sebum production via targeting stress signaling remains relatively limited. In this study, we investigated whether Camellia nitidissima flower extract (CNF) could counteract stress-induced sebaceous dysfunction and its underlying mechanisms. Using a cortisone-stimulated SZ95 human sebocyte model, we evaluated lipid accumulation, cortisol production, signaling pathway activation, and apoptotic markers. CNF treatment dose-dependently suppressed cortisone-induced lipid production, reducing triglyceride, cholesterol, and free fatty acid levels by up to 35.44%, 38.02%, and 46.39%. Mechanistically, CNF inhibited 11β-HSD1 expression (17.17% reduction) and cortisol secretion (32.84% decrease), thereby blocking local cortisol reactivation. This upstream interception subsequently attenuated PI3K/Akt/mTOR hyperphosphorylation, downregulated lipogenic transcription factors (SREBP-1, PPARγ, LXRα, C/EBP-α) and their target enzymes (FAS, ACC, DGAT). Beyond lipid synthesis inhibition, CNF reversed cortisone-induced apoptosis resistance by reducing the Bcl-2/Bax ratio and suppressing PCNA-mediated hyperproliferation, thereby decreasing sebocyte number. These findings demonstrate that CNF exerts dual oil-control effects: reducing lipid production per cell and reducing lipid-producing cell abundance. Collectively, CNF represents a promising multi-target botanical agent for managing stress-related sebaceous disorders and cosmetic sebum regulation.

Conventional perming relies on oxidative agents that significantly damage hair. The thiol–Michael click perming strategy derived from linear aliphatic diols and diamines has been developed to avoid oxidative damage, but lacks repeatable perming capabilities. In this study, a novel thiol–Michael click perming molecule was proposed for repeatable perming while avoiding oxidative damage. N,N′-bis(maleoyl)-l-cystine (MA2-CySS) was synthesized and characterized through Raman spectroscopy and ¹H NMR with MTT assay demonstrated no cytotoxicity up to 1000 μg/mL. Click reactivity analysis revealed that the reaction reached a plateau after 30 min, with alkaline pH and elevated temperatures significantly enhancing reactivity. MA2-CySS perming achieved efficiency comparable to oxidative perming, exceeding 1300% across three perming cycles. MA2-CySS perming significantly reduced both color change and cuticle damage, as demonstrated by color difference measurements and SEM, while maintaining superior mechanical properties as revealed by tensile property tests. Raman spectroscopy demonstrated that MA2-CySS perming better preserves hair keratin’s secondary structure, maintaining superior α-helix content at 27.50% versus 24.35%, exhibiting higher disulfide bond retention at 85% versus 72%, and showing gauche–gauche–gauche to trans–gauche–trans conformational conversion at 9% versus 6%. This study demonstrates that repeatable perming via thiol–Michael click reaction represents a significant advancement in perming methodology.

Platycladus orientalis exhibits significant potential as an antioxidant, anti-inflammatory, and hair growth-promoting ingredient, while the low bioavailability of raw Platycladus orientalis leaves extracts limits their further application. In this study, yeast fermentation was employed to prepare Platycladus orientalis Leaves Yeast Fermented Solution (PYFS). Its performance on human dermal papilla cells (HDPCs) was systematically investigated. The optimal fermentation strain was screened using the methyl thiazolyl tetrazolium (MTT) assay, and Saccharomycopsis fibuligera CICC33226 (SF) was identified as the most suitable strain for fermentation. The effects of PYFS on the cell cycle distribution, growth factors, inflammatory factors of HDPCs, as well as its hair growth-promoting mechanism, were investigated. Experiments revealed that after fermentation, the proportion of cells in the G0/G1 phase decreased by 11.09%, while the proportion of cells in the S phase increased by 35.44%. Additionally, the level of the growth factor VEGF increased by 42.34%, while the level of the inflammatory factor TGF-β1 decreased by 23.81%. Moreover, the fermentation process correlates with altered mRNA expression of Wnt/β-catenin pathway-related genes by upregulating the mRNA expression levels of β-catenin, DVL1, and LEF1, and downregulating the mRNA expression level of DKK-1. Finally, non-targeted metabolomics technology was used to analyze the metabolite changes after fermentation. The most significant differential metabolites mainly include flavonoids, amino acids and their derivatives, and organic acids and their derivatives. This study utilized microbial fermentation technology to prepare the yeast fermentation solution, selected the optimal fermentation strain, and demonstrated that its fermentation product significantly promotes HDPC metabolic activity, supports hair follicle health by regulating the balance of growth factors, alters expression patterns of Wnt/β-catenin pathway-related genes, and substantially alters the metabolite composition of Platycladus orientalis leaves extract through fermentation.

Biosurfactants are attracting much interest due to their potential application as therapeutic agents in the medical and cosmetic field. Previous studies have demonstrated that biosurfactant such as sophorolipid (SL) exhibits immunomodulatory effects. In this article, we found the potential of sophorolipid for inhibiting histamine-induced itch and preliminarily explored its molecular basis. First, behavioral tests indicated that SL can remit the histamine-induced scratching behaviors of mice. Second, SL can suppress the the calcium influx induced by histamine, HTMT and VUF8430 in HaCaT cells. RT-PCR analysis showed that the histamine-induced upregulation of mRNA levels of phospholipase Cγ1, 1,4,5-trisphosphate receptor (IP3R), and protein kinase Cα can be inhibted by SL, suggesting that SL may impede the PLC/IP3R signaling pathway activated by histamine. In further tests, the capsaicin-induced calcium influx can also be inhibited by SL. The immunofluorescence and molecular docking analysis indicated that SL acts as an inhibitor of transient receptor potential vanilloid-1 (TRPV1) activation to decrease calcium influx against stimuli. In summary, these results revealed that SL may inhibit histamine-induced itch by decreasing PLC/IP3R signaling pathway activation and modulating TRPV1 activity. This paper indicates that SL can be a useful treatment for histamine-dependent itch.

Autocrine and paracrine factors play key roles in the process of Androgenetic alopecia (AGA), which are secreted by balding dermal papilla cells (DPCs) after dihydrotestosterone (DHT) induction. Camellia seed cake is an oriental oil extraction byproduct, and its extract has been traditionally used to wash hair in China. This study elucidated the hair growth-promoting effects of Camellia seed cake extract (CSCE) in DHT-treated cultured DPCs and its underlying mechanisms. The effect of CSCE on cell viability and release of inflammatory factors IL-6 and IL-1α was performed on human dermal papilla cells (DPCs) incubated with DHT. Relative expression of bax, bcl-2, p53, androgen receptor (AR) and 5α- reductase type II (SRD5A2) was determined by PCR. Senescence-associated was examined by β-galactosidase (SA-β-Gal) assays. CSCE restored DHT-induced cell damage in a dose-dependent manner, and effectively reduced the production of IL-6 and IL-1α in DHT-treated DPCs. CSCE exhibited an anti-apoptotic effect, which increased the expression of bcl-2, and decreased the expressions of bax and p53 in DHT-incubated DPCs. CSCE also showed an anti-androgenic effect reversing the increase in AR and SRD5A2 expressions in DPCs driven by DHT incubation. In addition, CSCE inhibited the β-galactosidase enzyme activity and slowed down the cell senescence of DPCs which is crucial for AGA progression. In this study, we found that CSCE may have the potential to prevent and alleviate AGA by abrogating the effect of DHT in cultured DPCs.

Objectives: Biosurfactants with anti-inflammatory activity may alleviate skin irritation caused by synthetic surfactants in cleaning products. Sophorolipid (SL) is a promising alternative to synthetic surfactants. However, there are few reports on the anti-inflammatory activity of SL and the underlying mechanism. The purpose of this work is to verify that lipopolysaccharide (LPS)-induced inflammation could be inhibited through targeting the pathway of nuclear factor-κB (NF-κB) in RAW264.7 cells. Methods: The influence of SL on cytokine release was investigated by LPS-induced RAW264.7 cells using ELISA. The quantification of the protein expression of corresponding molecular markers was realized by Western blot analysis. Flow cytometry was employed to determine the levels of Ca²⁺ and reactive oxygen species (ROS). The relative expression of inducible nitric oxide synthase (INOS) and cyclooxygenase-2 (COX-2) was determined by RT-PCR. An immunofluorescence assay and confocal microscope were used to observe the NF-κB/p65 translocation from the cytoplasm into the nucleus. The likely targets of SL were predicted by molecular docking analysis. Results: SL showed anti-inflammatory activity and reduced the release of inflammatory cytokines including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and nitric oxide (NO). The experimental results show that SL suppressed the Ca²⁺ and ROS levels influx in the LPS-induced RAW264.7 cells and alleviated the LPS-induced expression of iNOS and COX-2, the LPS-induced translocation of NF-κB (p65) from the cytoplasm into the nucleus, and the expression of phosphorylated proteins such as p65 and IκBα. Furthermore, molecular docking analysis showed that SL may inhibit inflammatory signaling by competing with LPS to bind TLR4/MD-2 through hydrophobic interactions and by inhibiting IKKβ activation through the hydrogen bonding and hydrophobic interactions. Conclusion: This study demonstrated that SL exerted anti-inflammatory activity via the pathway of NF-κB in RAW264.7 cells.