Effect of Aralia Cordata Pharmacopuncture on Cartilage Protection and Apoptosis Inhibition In Vitro and in Collagenased-induced Arthritis Rabbit Model

Osteoarthritis is characterized by cartilage degradation and chondrocytes death. Chondrocyte death is induced by the apotosis through special mechanisms including the activation of caspase-3. On the basis of this background, this study was designed to examine the cartilage protective and anti-apototic effects of Aralia Cordata in in vtro and in collagenase-induced arthritis rabbit model. To conduct in vitro study, chondrocytes culturedfrom rabbit knee joint were treated by 5 ng/ml IL-1a.For in vivo experiment, collagenase-induced arthritis (CIA) rabbit model was made via intraarticular injection with 0.25 ml of collagenase solution. Aralia cordata pharmacopuncture (ACP) was administrated on bilateral Dokbi acupoint (ST35) of rabbits at a dosage of 150 ${\mu}g/kg$ once a day for 28 days after the initiation of the CIA induction. In the study by using CIA rabbit model in vivo, ACP showed the inhibition of cartilage degradation in histological analysis. Aralia cordata also showed anti-apoptotic effect both in vitro and in vivo study. In chondrocytes treated by IL-1a, Aralia cordata inhibited caspase-3 activity and enhanced the proliferation of IL-1a-induced dedifferentiated chondrocytes. ACP showed the inhibition effect on the caspase-3 expression and activity from CIA rabbit model. This study indicates that ACP inhibits the cartilage destruction and the chondrocyte apotosis through downregulation of caspase-3 activity. These data suggest that ACP has a beneficial effect on preventing articular cartilage destruction in osteoarthrtis.