Rabbit Chondrocytes

Effect of Farnesol and Farn/HA Nanoparticle on Cell Viability of Rabbit Chondrocytes

Osteoarthritis (OA) is a disease that involves the destruction of articular cartilage. The phenotype and metabolism of chondrocytes are the key of cartilage function. Dedifferentiation, the loss of chondrocyte phenotype and the synthesis of collagen I and X, is a common feature of OA chondrocytes in vitro. Farnesol possesses anti-inflammatory and pro-collagen synthesis properties but its effect on chondrocyte differentiation has not been fully investigated. Wu's group reported an in vitro study to test the potential of farnesol to reverse dedifferentiated chondrocytes' phenotype by measuring the collagen and glycosaminoglycan (GAG) synthesis.

The impact of Farnesol and Farn/HA nanoparticles on cell viability was assessed by MTT assay (Fig. 1A). Farnesol at concentrations of less than 0.4 mM was not significantly detrimental to cell viability after 24 hours. The half inhibitory concentration (IC₅₀) of farnesol was approximately 0.45 mM. The Farn/HA nanoparticles had an average diameter of 58.0 ± 10.4 nm (Fig. 1B), and an encapsulation efficiency (EE) of approximately 90% for farnesol. Approximately 90% of farnesol was released within 10 hours in phosphate-buffered solution (Fig. 1C). However, co-incubation with 4 mM Farn/HA nanoparticles was significantly detrimental to cell viability (Fig. 1D). The IC₅₀ of Farn/HA nanoparticles was approximately 1.9 mM, which is 4.2-fold higher than that of farnesol. These data suggest that HA nanoparticles may abrogate part of the inhibitory effect on cell viability and increase the therapeutic effect by slowing the release of the drug.

ALB-PRF Conditioned Media Promoting Proliferation, Migration and Adhesion of Rabbit Chondrocytes

Cartilage injury is prevalent in orthopedics, and cartilage tissue engineering offers a therapeutic direction for regeneration. Albumin (ALB)-platelet-rich fibrin (PRF) is theorized as an ideal natural scaffold for cartilage tissue engineering due to its origin from human venous blood. Zeng's team investigated the potential of ALB-PRF as a scaffold material through in vitro and in vivo experiments.

To study the effects of ALB-PRF on chondrocytes, they cultured these cells with different concentrations of ALB-PRF conditioned media. EdU staining showed that 20% ALB-PRF media significantly promoted cell proliferation in a concentration-dependent manner (Fig. 2A, B). The CCK8 assay also confirmed the proliferative effects of ALB-PRF (Fig. 2C). Additionally, transwell experiments showed that ALB-PRF media significantly enhanced chondrocyte migration, also in a concentration-dependent way, though FBS had the strongest effect (Fig. 2D, F). To see if ALB-PRF could serve as a scaffold material for tissue engineering, we tested its ability to support cell adhesion and growth. Cells were directly inoculated onto ALB-PRF and cultured for 10 days. HE staining showed that as the concentration of growth factors increased, cells not only adhered to the ALB-PRF surface but also grew into the inner zone of the gel, degrading the surrounding ALB (Fig. 2E, G).