IL-1ß induces apoptosis and autophagy via mitochondria pathway in human degenerative nucleus pulposus cells.

IL-1ß has been reported highly expressed in degenerative intervertebral disc, and our previous study indicated IL-1ß facilitates apoptosis of human degenerative nucleus pulposus (NP) cell. However, the underlying molecular mechanism remains unclear. We here demonstrate that IL-1ß played a significantly pro-apoptotic effect under serum deprivation. IL-1ß decreased Bcl-2/Bax ratio and enhanced cytochrome C released from mitochondria to cytosol, which proved mitochondria-meidated apoptosis was induced. Subsequently, mitochondria damage was detected under IL-1ß stimualtion. In addition, IL-1ß-mediated injuried mitochondria contributes to activate autophagy. However, pretreatment with the autophagy inhibitor 3-methyladenine showed the potential in further elevating the apoptosis rate induced by IL-1ß in NP cells. Our results indicated that the mitochondrial pathway was involved in IL-1ß-induced apoptosis of NP cells. Meanwhile, the damaged mitochondria-induced autophagy played a protective role against apoptosis, suggesting a postive feedback mechanism under inflammatory stress.