Caspase 3 Silencing Inhibits Biomechanical Overload-induced Intervertebral Disc Degeneration

椎间盘（IVD）退变导致衰弱腰痛在世界范围内的大部分人口。由于发病机制尚不清楚，目前尚无有效的治疗方法。变性早期的一个特征性事件是IVD内嵌的髓核（NP）细胞凋亡。过度的生物力学负荷也可能是IVD退行性变的主要原因。本研究采用体外和体内压缩载荷模型来阐明IVD变性的潜在机制。此外，我们研究了抑制细胞凋亡是否是治疗生物力学应力诱导的IVD变性的潜在临床治疗策略。本研究表明，caspase 3 siRNA通过抑制NP细胞凋亡和基质降解酶的表达来减轻超载诱导的IVD变性。

Intervertebral disc (IVD) degeneration causes debilitating low back pain in large sections of the worldwide population. No efficient treatment currently exists because the unclear pathogenesis. One characteristic event early in the degeneration is the apoptosis of nucleus pulposus (NP) cells embedded in IVD. Excessive biomechanical loading may be also a major etiology of IVD degeneration. The present study used in vitro and in vivo models of compressive loading to elucidate the underlying mechanism of IVD degeneration. In addition, we investigated whether the inhibition of apoptosis is a potential clinical therapeutic strategy for the treatment of IVD degeneration induced by biomechanical stress.The present study suggests that caspase 3 siRNA attenuates overload-induced IVD degeneration by inhibiting NP cell apoptosis and the expression of matrix-degrading enzymes.