Osteoarthritis (OA) is a chronic disease characterized by cartilage degradation, leading to bone friction, inflammation, stiffness, pain, and reduced mobility. This study investigates the therapeutic effects of porcine-derived chondroitin sulfate sodium (CS) on OA symptoms at both cellular and animal levels. In vitro study, HTB-94 chondrocytes were treated with inflammatory stimuli and CS (10, 50, 100, and 200 μg/mL) to assess the release of inflammatory mediators and the expression of genes and proteins related to cartilage synthesis and degradation. In vivo study, an MIA-induced OA rat model was used, and CS (62, 124, and 248 mg/kg b.w.) was orally administered for 4 weeks. Key parameters, such as exercise capacity, micro-CT, histological evaluation of joint tissues, serum inflammatory markers, and the expression of mRNA and proteins (inflammatory, cartilage synthesis and degradation, and apoptosis markers), were analyzed. Porcine-derived CS significantly reduced PGE₂, NO, and extracellular matrix degradation marker (COMP and CTX-II) levels and increased the expression of cartilage synthesis-related genes and proteins in both HTB-94 cells and the MIA-induced rats. Additionally, CS modulated cartilage degradation pathways and notably inhibited apoptosis in vivo. The effects of porcine CS were comparable to the NSAID ibuprofen, demonstrating its potential as an anti-inflammatory and chondroprotective agent for OA management and dietary supplementation.

Collagen peptides have been widely studied for their beneficial effects on skin health; however, their potential role in hair growth remains insufficiently explored. This study aimed to investigate the effects of orally administered low-molecular-weight fish collagen peptide (SH-GT) on hair regrowth and its underlying mechanisms in a hair-removed C57BL/6J mouse model. Mice were administered SH-GT (100, 300, or 600 mg/kg body weight) or a positive control (Pansidil, 400 mg/kg) daily for 28 days. SH-GT significantly enhanced hair regrowth, as evidenced by the increased hair growth area. Histological analysis revealed increased dermal thickness and visible hair follicle structures in SH-GT-treated groups. At the molecular level, SH-GT upregulated proliferation-related proteins, including PCNA and Cyclin D1, and activated Wnt/β-catenin signaling. In addition, SH-GT enhanced PI3K/Akt/mTOR signaling, suggesting improved cellular growth and survival. Conversely, SH-GT suppressed hair growth inhibitory pathways by reducing BMP4 expression and decreasing Smad phosphorylation. Furthermore, SH-GT increased the mRNA expression of growth factors such as IGF-1, HGF, VEGF, EGF, and FGF7. In conclusion, SH-GT promotes hair regrowth by simultaneously activating proliferation-related signaling pathways and suppressing inhibitory mechanisms, thereby improving the dorsal skin microenvironment associated with hair regrowth. These findings suggest that SH-GT may serve as a promising functional ingredient for improving hair growth.

Age-related cognitive impairment is often linked to cholinergic dysfunction and increased oxidative stress. This study explored the neuroprotective potential of lutein–zeaxanthin extract (XanMax ^® 2002; LZ) through both in vitro and in vivo approaches. In vitro , Neuro-2a cells exposed to hydrogen peroxide (H ₂ O ₂ ) were treated with LZ (5–20 μg/mL), leading to decreased expression of apoptosis-related proteins. In vivo , memory impairment was induced by scopolamine in C57BL/6N mice, followed by oral administration of LZ (4 or 8 mg/kg) for 4 weeks. Behavioral assessments—including the Morris water maze, Y-maze, and passive avoidance tests—demonstrated significant improvements in spatial learning, working memory, and memory retention in LZ-treated groups, particularly at the higher dose. Biochemical analysis revealed increased acetylcholine levels, reduced acetylcholinesterase activity, and downregulation of oxidative stress and neuroinflammatory markers in brain tissue. Moreover, LZ supplementation upregulated genes associated with synaptic function and memory. The cognitive-enhancing effects of LZ were comparable with those of donepezil. These findings suggest that LZ may exert neuroprotective effects through antioxidant and anti-inflammatory mechanisms and are a potential dietary intervention for cognitive decline.