Abstract

Knee osteoarthritis (KOA) is a prevalent joint disorder characterized by articular cartilage degeneration and apoptosis. This research was aimed to demonstrate effects of calcitonin (CT) on apoptosis and Bcl-2 in KOA articular chondrocytes. In vitro cellular experiments were conducted using articular chondrocytes obtained from KOA patients, with a portion of the cells undergoing passaging and proliferation culture. The remaining cells were rolled into control group (normal chondrocytes), KOA group (chondrocytes from arthritis joints), and CT group (chondrocytes from arthritis joints treated with CT). Control and KOA groups were treated with an equivalent amount of saline solution. Apoptosis and Bcl-2 protein expression levels were assessed in each group to evaluate the impact of CT on articular chondrocytes. It was revealed that proliferation rate of human chondrocytes decreased with increasing passage number, and the exponential growth phase was shorter. After day 6, the proliferation rate drastically increased, exhibiting an exponential growth trend. Relative to KOA group, the CT group demonstrated a notable reduction in apoptosis of articular chondrocytes (P <0.05). Bcl-2 protein level was greatly upregulated in CT group (P < 0.05). In short, CT can inhibit apoptosis of articular chondrocytes and promote Bcl-2 expression, thereby contributing to the stability and survival of articular chondrocytes. In summary, CT has a positive effect on apoptosis and Bcl-2 expression in KOA articular chondrocytes.

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