Baicalin suppresses interleukin-1β-induced apoptosis, inflammatory response, oxidative stress, and extracellular matrix degradation in human nucleus pulposus cells

Objective To explore the effect of baicalin on human nucleus pulposus cells (NPCs) in response to IL-1β stimulation.Methods Viability of NPCs was measured by CCK-8 assay. TUNEL staining assay and flow cytometry were performed to detect apoptotic cell death of NPCs. Western blot analysis was conducted to detect the expression levels of proteins. ELISA was applied for the determination of iNOS, COX-2, TNF-α and IL-6. Oxidative stress indicators including ROS production, MDA level, and SOD activity were measured.Results Baicalin attenuated IL-1β-caused cell viability reduction and Apoptosis in NPCs. IL-1β-induced increase in Bax expression and decrease in Bcl-2 expression were attenuated by baicalin treatment. IL-1β-induced production of iNOS, COX-2, IL-6 and TNF-α in NPCs were inhibited by baicalin treatment. Baicalin treatment reversed IL-1β-induced increase in ROS production and MDA level, as well as decrease in SOD activity. Furthermore, baicalin treatment elevated the expression levels of Col II and Aggrecan and downregulated the expression levels of MMP3, MMP13, and ADAMTS5 in IL-1β-induced NPCs. A total of 402 related targets of baicalin and 134 related targets of intervertebral disc degeneration were found, and 9 intersection targets were screened out. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that MAPK pathway was found to be involved in the effects of baicalin.Conclusions Baicalin exhibited protective effects on IL-1β-caused cell viability reduction, Apoptosis, oxidative stress, inflammation, and extracellular matrix degradation in NPCs. In addition, we found JNK and p38 MAPK pathways as targets of baicalin through bioinformatic analysis.

IL-1β; MAPK signaling pathway; baicalin; human nucleus pulposus cells; intervertebral disk degeneration (IDD).