Objective：To investigate the protective effects of adiponectin（APN）on apoptosis and extracellular matrix（ECM）degradation in rat nucleus pulposus（NP） cells under oxidative stress. Methods：Cell viability was detected by cell counting kit-8（CCK-8）to determine the optimal protective concentration of APN. Cells were randomly divided into the control group，the H2O2 group，the APN+H2O2 group and the compound C+APN+H2O2 group. Apoptosis incidence was evaluated by flow cytometry. The expression of Bcl-2，Bax，cleaved caspase-3，matrix metalloproteinase-13（MMP-13） and a disintegrin and metalloproteinase with thrombospondin motifs-5（ADAMTS-5）was detected by Western blot. The mRNA levels of collagen type Ⅱ alpha 1 chain（COL2A1） and aggrecan（ACAN） were detected by RT-PCR. The phosphorylation levels of adenosine 5′-monophosphate-activated protein kinase（AMPK）and mammalian target of rapamycin（mTOR） were evaluated by Western blot. Results：One μg/mL APN conferred the optimal protection against the cytotoxicity of 200 μmol/L H2O2. APN pretreatment significantly suppressed H2O2-induced apoptosis in NP cells. Consistently，the increase in Bax/Bcl-2 ratio and the expression of cleaved caspase-3 was also inhibited by APN. Although no notable inhibitory effect on ADAMTS-5 was observed，APN reduced the expression of MMP-13 induced by H2O2. Besides，the inhibition of H2O2 on the transcription of COL2A1 and ACAN was also notably abated by APN. APN also induced the phosphorylation of AMPK and suppressed the phosphorylation of mTOR. Inhibition of AMPK with compound C alleviated the suppression of APN on mTOR phosphorylation. Moreover，the inhibition of APN on apoptosis and catabolism，together with the promotion of APN on anabolism were also reversed by compound C. Conclusion：APN inhibits H2O2-induced apoptosis and ECM degradation in rat NP cells in an AMPK/mTOR dependent manner.