The objective of this study was to investigate the effect of low-molecular-weight fish collagen (valine-glycine-proline-hydroxyproline-glycine-proline-alanine-glycine; LMWCP) on H₂O₂- or LPS-treated primary chondrocytes and monoiodoacetate (MIA)-induced osteoarthritis rat models. Our findings indicated that LMWCP treatment exhibited protective effects by preventing chondrocyte death and reducing matrix degradation in both H₂O₂-treated primary chondrocytes and cartilage tissue from MIA-induced osteoarthritis rats. This was achieved by increasing the levels of aggrecan, collagen type I, collagen type II, TIMP-1, and TIMP-3, while simultaneously decreasing catabolic factors such as phosphorylation of Smad, MMP-3, and MMP-13. Additionally, LMWCP treatment effectively suppressed the activation of inflammation and apoptosis pathways in both LPS-treated primary chondrocytes and cartilage tissue from MIA-induced osteoarthritis rats. These results suggest that LMWCP supplementation ameliorates the progression of osteoarthritis through its direct impact on inflammation and apoptosis in chondrocytes.

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.

This study investigated the protective effects of a ceramides derivates from the peach (PF3) on photoaging by UV-irradiated hairless mice. Mice were randomly divided into seven groups: AIN93G without UVB exposure (normal control, NC), AIN93G with UVB exposure (control, C), AIN93G supplemented 100 mg/kg body weight (BW) of L-ascorbic acid with UVB exposure (AA), AIN93G supplemented 100 mg/kg BW of arbutin with UVB exposure (Arbutin), AIN93G supplemented 10 mg/kg BW of PF3 with UVB exposure (10PF3), AIN93G supplemented 20 mg/kg BW of PF3 with UVB exposure (20PF3), and AIN93G supplemented 40 mg/kg BW of PF3 with UVB exposure (40PF3). The study examined the impact of PF3 on skin hydration, wrinkle formation, and melanogenesis using enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (real-time PCR), and Western blot analysis. The PF3 demonstrated significant protective effects against photoaging by reducing skin wrinkle formation, decreasing epidermal and dermal thickening, and improving skin hydration. It also enhanced the expression of moisture-related factors (hyaluronic acid synthase [HAS], long-chain ceramides [LCBs], dihydroceramide desaturase 1 [DEGS1], and type I collagen [COL1A]) and antioxidant enzyme activities while reducing pro-inflammatory cytokines and oxidative stress markers. The PF3 supplementation positively modulated skin wrinkle formation-related factors, increasing collagen-related gene expression and decreasing matrix metalloproteinases. Additionally, PF3 showed potential in regulating melanogenesis by reducing the nitric oxide and cAMP content, as well as the expression of melanogenesis-related proteins. These comprehensive findings suggest that PF3 supplementation may be an effective strategy for preventing and treating UVB-induced skin photoaging through multiple mechanisms, including improved skin structure, hydration, antioxidant defense, and reduced inflammation and pigmentation.