OBJECTIVES: Kashin-Beck disease (KBD) is an endemic osteoarthropathy.This study is to observe the change of NF-κB signaling in KBD patients and expression of NF-κB p65 in human C28/I2 chondrocyte for analyzing the effect of NF-κB p65 on chondrocyte apoptosis.

METHODS: RESULTS: Compared with age and sex, differences were not statistically significant between KBD group and control group (t=0.336，P=0.737；χ=0.407，P=0.523). The protein expression level of NF-κB p65 in KBD group was 1.833 times as high as that of control group (P<0.05). In C28/I2 chondrocyte oxidative damage model, the number of cell apoptosis increased in tBHP group and level of ROS and protein expression level of NF-κB p65 were higher than that of control group (P<0.05), however, levels of ROS were lower than that of control group (P<0.05), protein levels of NF-κB p65 were down-regulated in low and middle selenium pre-protection group compared to tBHP group (P>0.05).

CONCLUSIONS: The NF-κB signaling pathway is up-regulated in KBD patients, moreover, chondrocyte experiments showed cell apoptosis was mediated via up-regulation of NF-κB p65, and the expression of p65 is down-regulated by NaSeOintervention, which suggest NF-κB signaling pathway play an important role in pathogenesis of KBD (This research was supported by National Natural Science Foundation in China No.81573104,81172610, 81673117).