| Objective To observe the effect of salidroside on apoptosis and inflammatory response of degenerated nucleus pulposus cells and to explore its relationship with JAK2/STAT3 signaling pathway. Methods The degenerated nucleus pulposus cell model was established by oxidative glucose deprivation (OGD) culture. The degeneration cells were cultured in addition of 10 ?g/ml, 30 ?g/ml, or 50 ?g/ml of salidroside, respectively. Cells in 30ug/ml of salidroside were used in the follow-up experiments. They were divided into control group, OGD group, salidroside group, AG490 (inhibitor of JAK2/STAT3 signaling pathway) group, and salidroside combined with AG490 intervention group. The mRNA expression of aggrecan and Col2a1 in nucleus pulposus cells was detected by RT-PCR. Western blotting was used to detect the effects of salidroside on p-JAK2 and p-STAT3 protein levels in nucleus pulposus cells. The levels of TNF-α, IL-1β, and IL-6 in the supernatant were detected by ELISA. The apoptosis of nucleus pulposus cells was detected by flow cytometry. Results Compared with control group, the mRNA expression of aggrecan and Col2a1 in OGD group decreased significantly, but the levels of TNF-α, IL-1β, and IL-6 increased, and the protein levels of p-JAK2 and p-sTAT3 were significantly up-regulated. Compared with OGD group, salidroside significantly inhibited release of apoptosis and inflammation-related factors TNF-α, IL-1β and IL-6. Meanwhile, we found that the above indicators in AG490 group and salidroside combined with AG490 intervention group decreased significantly, and those in salidroside combined with AG490 intervention group were slightly lower than those in AG490 group. Salidroside combined with AG490 pretreatment significantly relieved the apoptosis and inflammation response of nucleus pulposus cells and inhibited the phosphorylation of JAK2 and STAT3. Conclusion Salidroside reduces the apoptosis and inflammation response of degenerative nucleus pulposus cells by inhibiting the activation of JAK2/STAT3 signaling pathway. |