Adiponectin Downregulates TNF-α Expression in Degenerated Intervertebral Discs.

STUDY DESIGN: Given the results of previous in vitro investigations of the expression patterns of adiponectin and its receptors in healthy and degenerated intervertebral discs (IVDs), we studied the effects of adiponectin on tumor necrosis factor-alpha (TNF-α) production in degenerated nucleus pulposus (NP) cells and analyzed the association between adiponectin levels in IVD tissues and IVD Pfirrmann grades.

OBJECTIVE: The aim of this study was to investigate the potential role of adiponectin in the pathogenesis of IVD degeneration.

SUMMARY OF BACKGROUND DATA: Adiponectin has been reported to be involved in physiologic and pathologic processes associated with bone and cartilage diseases. However, the expression profiles of adiponectin and its receptors in human IVD tissues and the function of adiponectin in the pathogenesis of IVD degeneration remain unknown.

METHODS: Real-time polymerase chain reaction, immunohistochemistry, and western blotting were performed to examine the expression levels of adiponectin, adiponectin receptors, and TNF-α in IVD tissues and isolated NP cells. The effects of adiponectin on TNF-α production in degenerated NP cells were detected by enzyme linked immunosorbent assay.

RESULTS: Adiponectin expression levels were downregulated, while adiponectin receptor 1 (adipoR1) and adipoR2 expression levels were upregulated in degenerated IVD tissues and degenerated NP cells compared with those in healthy IVD tissues and healthy NP cells. Moreover, we confirmed that TNF-α production by degenerated NP cells was downregulated by adiponectin administration in a dose- and time-dependent manner. Furthermore, our data showed that adiponectin levels in degenerated IVD tissues were inversely correlated with IVD Pfirrmann grades.

CONCLUSION: These results indicated that adiponectin may play an anti-inflammatory role with respect to the maintenance of IVD homeostasis by downregulating TNF-α production.

LEVEL OF EVIDENCE: N/A.