Apelin-13/APJ system delays intervertebral disc degeneration by activating the PI3K/AKT signaling pathway.

Objective To study the effect of Apelin-13/APJ system on intervertebral disc degeneration and its mechanism. Patients and methods This study detected the expression of APJ in human intervertebral disc tissue with varying degrees of degeneration. IL-1β is used to stimulate the degeneration of nucleus pulposus cells. We used recombinant human Apelin-13 and Ala13 to activate and inhibit the APJ receptor, respectively. The inhibitor LY294002 was used to inhibit the PI3K/AKT signaling pathway. We studied the effects of Apelin-13/APJ system on nucleus pulposus cells and its mechanism by Western blot, RT-PCR, and so on. Results APJ is lowly expressed in the nucleus pulposus of patients with a high degree of degeneration. IL-1β stimulates the nucleus pulposus cells and reduces the expression of APJ in nucleus pulposus cells. Recombinant human Apelin-13 reduces the degradation of nucleus pulposus extracellular matrix, promotes proliferation, and reduces the levels of apoptosis and inflammation. In addition, the Apelin-13/APJ system increases the expression of PI3K and AKT and activates the PI3K/AKT signaling pathway. Conclusions Apelin-13/APJ system activates PI3K/AKT signaling pathway activity, reduces the degradation of nucleus pulposus extracellular matrix, promotes proliferation, and reduces the level of apoptosis and inflammation, thus delaying the degeneration of the intervertebral disc.