Background: Arctigenin (ATG) is the active ingredient of the Chinese herbal medicine Arctium lappa, with anti-inflammatory and antioxidant effects. Excessive inflammation and cell apoptosis are important causes of intervertebral disc degeneration (IDD). Hence, this study probed into the possible role of ATG in IDD.
Methods: Interleukin (IL)-1β (10 ng/ml) was adopted to induce human nucleus pulposus cells (HNPCs) as a cell model for IDD. The effects of different concentrations of ATG (0, 2, 5, 10, 20, 50 μmol/L) on the viability of HNPCs and effects of ATG (10, 50 μmol/L) on the viability of IL-1β-induced HNPCs were detected by cell counting kit-8 (CCK-8). After IL-1β-induced HNPCs were transfected with miR-483-3p inhibitor and/or treated with ATG, cell viability and apoptosis were determined by CCK-8 and flow cytometry; the expressions of miR-483-3p, extracellular matrix (ECM)-related genes, and inflammation-related genes were measured by quantitative real time polymerase chain reaction (qRT-PCR), and expressions of ECM/apoptosis/NF-κB pathway-related proteins were quantified by Western blot.
Results: ATG had no significant effect on the viability of HNPCs but could promote the viability of IL-1β-induced HNPCs. ATG inhibited apoptosis, ECM degradation, inflammation, and activation of NF-κB pathway in HNPCs induced by IL-1β, but promoted the expression of miR-483-3p. MiR-483-3p inhibitor reversed the above-mentioned regulatory effects of ATG.
Conclusion: Arctigenin suppresses apoptosis, ECM degradation, inflammation, and NF-κB pathway activation in HNPCs by up-regulating miR-483-3p.
Keywords: arctigenin; human nucleus pulposus cells; intervertebral disc mutation; miR-483-3p.
© 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.