Glycyrrhizin suppresses inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JUK signaling pathway in attenuating intervertebral disc degeneration

• Published in: American journal of translational research Vol. 11; no. 8; pp. 5105 - 5113
• Main Authors: Liu, Xiao, Zhuang, Jian, Wang, Deguo, Lv, Lanxin, Zhu, Fenghui, Yao, Aiming, Xu, Tie
• Format: Journal Article
• Language: English
• Published: United States e-Century Publishing Corporation 01.01.2019
• Subjects: Original; intervertebral disc degeneration; HMGB1; inflammation; glycyrrhizin; Nucleus pulposus cells
• ISSN: 1943-8141; 1943-8141

Intervertebral disc degeneration (IDD) is associated with the nucleus pulposus (NP) cells inflammation and apoptosis. Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition. However, it is not known whether GL protects against IDD by the inhibition of HMGB1. To study the effect and mechanism of glycyrrhizin on intervertebral disc degeneration. We analyzed the expression of HMGB1 in different degree of degenerate disc tissues. Interleukin 1 beta (IL-1β) was used in stimulating the NP cells to degeneration. We used recombined human HMGB1 to resist the function of GL to explore whether GL acted via the target of HMGB1. Our study showed that the expression of HMGB1 markedly increased in severely degenerated disc tissues. IL-1β promoted the progress of IDD, and the stimulation of GL could reverse the effects of IL-1β. Moreover, p38 and p-JNK were significantly suppressed by GL stimuli. These results suggested that GL prevented NP degradation via restraining inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JNK signaling pathway. GL may become a novel cytokine for the therapy of IDD in the future.