CUR treatment inhibits TBHP-induced ECM degradation, oxidative stresses, and mitochondrial dysfunction by facilitating autophagic flux. (a–g) The protein levels of type II collagen, aggrecan, MMP-3, MMP-13, ADAMTS-4, and ADAMTS-5 in the human NP cells were measured by western blotting. (h, i) The ROS levels were detected using the fluorescent probe DHE and measured by flow cytometry. (j) Intracellular MDA levels in the human NP cells. (k, l) Mitochondrial membrane potential was detected by JC-1 staining and measured by flow cytometry. (m) An assessment of mPTP opening in the human NP cells. (n) Intracellular ATP levels in the human NP cells. GAPDH was used as an internal control. Data are represented as the mean ± SD. ∗∗P < 0.01 versus control group. ##P < 0.01 versus TBHP group. &&P < 0.01, &P < 0.05 versus TBHP+CUR group, n = 3.