Abstract
The ankle biomechanics is easily changed due to the acute injury of the tissue around the ankle joint and the damage of the ankle joint structure, such as ankle instability and joint surface imbalance. When the mechanical load of the ankle changes, it can cause ankle regeneration and remodeling processes such as cartilage loss, bone remodeling, and degenerative changes. The aim of this study was to investigate the effect and mechanism of ginsenoside Rg1 against interleukin-1β (IL-1β)-induced apoptosis in human articular chondrocytes (HACs). The apoptosis model of HAC cells was established by IL-1β induction, and then the HAC cells were cultured with different concentrations of Rg1. The protective effect of Rg1 on HAC cell apoptosis was investigated by detecting the changes of apoptosis and activity of PI3K/Akt/mitochondrial signaling pathway. The results showed that a specific concentration of Rg1 could promote the proliferation of IL-1β-induced HAC cells and inhibit apoptosis. At the same time, Rg1 treatment with specific concentration can reduce the content of reactive oxygen species (ROS) and malondialdehyde (MDA) in HACs and improve the related expression of mitochondrial membrane potential (MMP). Furthermore, qRT-PCR and western blot results showed that Rg1 could improve the low expression of Bcl-2 and inhibit the high expression of Bax, caspase-3, caspase-8, caspase-9, FasL, AIF, and Cyto c in IL-1β-induced cells. In summary, Rg1 can inhibit IL-1β-induced apoptosis of HAC cells by decreasing the activity of PI3K/Akt/mitochondrial signaling pathway, and Rg1 has a protective effect on apoptosis of HAC cells.