Centella asiatica extract (CAE) and Marigold extract (ME) have been renowned for centuries in traditional medicine, particularly in Asia, for their wound‐healing, anti‐inflammatory and skin‐regenerative properties. This study presents the formulation and comprehensive evaluation of serums enhanced with these extracts, aiming to harness their bioactive properties for skin health. Serums were selected over creams due to their lightweight, water‐based nature, which ensures faster absorption and enhanced skin penetration of active ingredients. The serums, developed in varying concentrations (0.2%, 0.5% and 1.0%), were assessed for physicochemical properties, stability, bioactivity and skin barrier enhancement. Stability tests confirmed the serums' robustness, maintaining consistent pH (5.0–6.5), viscosity and organoleptic properties over 60 days. The MTT assay revealed that both extracts were non‐cytotoxic, maintaining cell viability above 100%, with formulations containing CAE, demonstrating a concentration‐dependent proliferative effect, reaching nearly 120%. Antibacterial evaluation using the agar well diffusion assay showed that both extracts exhibited considerable activity, with CAE achieving greater inhibition zones, particularly against S. aureus . Antioxidant, anti‐inflammatory and anti‐tyrosinase activities confirmed the strong bioactive potential of both extracts in combating oxidative stress, reducing inflammation, and regulating pigmentation. Skin barrier and permeability studies demonstrated the serums' ability to improve barrier integrity and facilitate active compound delivery. These findings demonstrate the potential of Centella asiatica and Marigold extracts for multifunctional skincare formulations, combining regeneration, hydration, antioxidant and antibacterial benefits.

Background/Objectives: Mesenchymal stem cells (MSCs) possess immunomodulatory properties, tumor-homing, and low immunogenicity, making them attractive for cell-based cancer therapies, but their role in colorectal cancer (CRC) remains controversial. The MSC1 phenotype, a pro-inflammatory, tumor-suppressive state induced by short-term, low-dose LPS activation via TLR4, has shown therapeutic promise but remains poorly characterized in CRC. We aimed to elucidate MSC1’s tumor-suppressive mechanisms and validate its activity against CRC cells using an integrated bioinformatics and in vitro approach. Methods: We constructed a high-confidence protein-protein interaction (PPI) network in Wharton’s jelly-derived MSCs (WJ-MSCs) following TLR4 activation to uncover enriched signaling pathways, transcriptional regulators, and secreted factors. Functional and transcriptional enrichment analyses pinpointed key mechanisms. We then co-cultured MSC1 cells with CRC cells to assess effects on proliferation and metabolism. Results: Network analysis revealed six tumor-suppressive mechanisms of MSC1 cells: (i) Metabolic reprogramming via enhanced glucose and lipid uptake, phosphoinositide signaling, and membrane/protein recycling, (ii) Robust antioxidant defenses, including SOS signaling and system xc⁻, (iii) Extracellular matrix stabilization and laminin-111–integrin-mediated adhesion, (iv) Secretome with direct anti-cancer effects, (v) Regulation of survival and cancer-associated fibroblasts (CAFs) formation inhibition through balanced proliferation, apoptosis, and epigenetic signals, (vi) Controlled pro-inflammatory signaling with anti-inflammatory feedback. In vitro, MSC1 cells significantly suppressed CRC cell proliferation and metabolic activity versus controls. Conclusions: This study provides the first mechanistic map of MSC1’s tumor-suppressive functions in CRC, extending beyond immunomodulation to include metabolic competition, ECM stabilization, and anti-cancer secretome activity. These findings establish MSC1 cells as a novel therapeutic strategy for CRC in cell-based cancer therapies.

Responses to cutaneous injury differ fundamentally across developmental stages in several mammal species. During early human gestation, when the fetus is less than 24 weeks old, wounds are capable of restoring normal tissue architecture without forming fibrotic scars. In contrast, postnatal and adult injuries typically resolve through the process of fibrosis. This divergence reflects coordinated differences in epidermal and dermal compartments, inflammatory signaling, extracellular matrix (ECM) composition, mechanical cues, and gene regulation. Recent studies have demonstrated that dermal fibroblasts are no longer considered a uniform population but instead arise from distinct developmental lineages with stable functional identities. Engrailed-1-negative fibroblasts (ENFs) predominate in early fetal skin in mice and support regenerative repair, while Engrailed-1-positive fibroblasts (EPFs) emerge later in development and are the principal contributors to fibrotic matrix deposition following injury. The developmental shift between these fibroblast populations coincides with the loss of scar-free healing capacity. This review examines the current understanding of fibroblast lineage specification, with particular emphasis on the roles of mechanotransduction, extracellular matrix cues, and epigenetic regulation. Elucidating how these lineage-encoded programs are established and maintained may enable strategies to reprogram adult fibroblasts toward a fetal-like regenerative state and thereby promote scar-free tissue repair.

Introduction: Multiple factors have been linked with increased risk of anastomotic leak in bowel surgery, including infections, inflammatory bowel disease, patient comorbidities and poor surgical technique. The aim of this study was to investigate the positive effect, if any, of adipose derived mesenchymal stem cells (MSCs) mixed with platelet-rich plasma (PRP) in the healing of bowel anastomoses, in an inflammatory environment after establishment of experimental colitis. Materials and Methods: Thirty-five male Wistar rats were divided into five groups of seven animals: normal controls, colitis controls, PRP, MSCs, and PRP+MSCs. All groups underwent laparotomy, one-cm segmental colectomy and anastomosis in situ. In the colitis group, colectomy was performed at the affected area. Colitis was previously established by transrectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) except for the normal controls. Post-mortem histopathological, tissue hydroxyproline and anastomotic bursting pressure (ABP) assessments were performed. The Mann–Whitney U test was used to assess statistical significance differences between groups. Results: No perioperative mortality was noted. Tissue hydroxyproline and ABP were significantly increased in the group of PRP+MSCs compared to colitis controls (p = 0.0151 and p = 0.0104, respectively). Inflammatory cell infiltration was lower and fibroblast activity higher in PRP+MSCs group, but not statistically significant (p > 0.05). Neoangiogenesis (p = 0.0073) and anastomotic area epithelialization (p = 0.0182) were significantly higher in PRP + MSCs group compared to colitis controls. Discussion: The synergistic effect of the PRP and MSCs is apparently responsible for the improved healing markers in bowel anastomoses even on inflammatory bowel. This gives hope for primary anastomoses and stoma saving in many emergency and/or elective circumstances, especially in immunocompromised or malnourished patients, even in cases with inflammation or peritonitis. Clinical studies should follow in order to support the clinical application of PRP+MSCs in gastrointestinal anastomoses.

Responses to cutaneous injury differ fundamentally across developmental stages. During early human gestation, when the fetus is less than 24 weeks old, wounds are capable of restoring normal tissue architecture without forming fibrotic scars. In con-trast, postnatal and adult injuries typically resolve through the process of fibrosis. This divergence reflects coordinated differences in epidermal and dermal compartments, inflammatory signaling, extracellular matrix (ECM) composition, mechanical cues, and gene regulation. Recent studies have demonstrated that dermal fibroblasts are no longer considered a uniform population but instead arise from distinct developmental lineages with stable functional identities. Engrailed-1–negative fibroblasts (ENFs) predominate in early fetal skin and support regenerative repair, while Engrailed-1–positive fibroblasts (EPFs) emerge later in development and are the principal contrib-utors to fibrotic matrix deposition following injury. The developmental shift between these fibroblast populations coincides with the loss of scar-free healing capacity. This review examines current understanding of fibroblast lineage specification, with par-ticular emphasis on the roles of mechanotransduction, ECM cues, and epigenetic reg-ulation. Elucidating how these lineage-encoded programs are established and main-tained may enable strategies to reprogram adult fibroblasts toward a fetal-like regen-erative state and thereby promote scar-free tissue repair.