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Updated: Oct 14, 2025

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
Ganoderic Acid A Attenuates IL-1β-Induced Inflammation in Human Nucleus Pulposus Cells Through Inhibiting the NF-κB
Sihua Zheng1, Jianmin Ma2, Xuezheng Zhao1
1Orthopedics Department, Xixi Hospital of Hangzhou, Hangzhou, 310023, China.
Abstract:
Intervertebral disc (IVD) degeneration is a major cause of low back pain associated with several pathological changes in the IVD, including dysfunction of nucleus pulposus (NP) cells. Ganoderic Acid A (GAA), one of triterpenoid extracts of Ganoderma lucidum (G. lucidum), has been reported to possess anti-inflammatory effect. In the current study, we aimed to evaluate the effect of Ganoderic Acid A (GAA) on the interleukin-1β (IL-1β)-induced inflammation in human NP cells. Our results showed that the IL-1β-stimulated production of inflammatory mediators including nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 were suppressed by GAA. In addition, treatment of NP cells with GAA significantly inhibited the production of inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in IL-1β-stimulated human NP cells. GAA improved the reduced expression levels of extracellular matrix (ECM) proteins, collagen II and aggrecan in IL-1β-stimulated human NP cells. GAA also alleviated IL-1β-induced the levels of matrix metalloproteinase (MMP)-3 and MMP-13. Furthermore, GAA inhibited the IL-1β-induced upregulation of the phosphorylation of p65 and downregulation of IκBα. Taken together, these findings indicated that GAA alleviated IL-1β-induced inflammation and ECM degradation in NP cells through regulating NF-κB pathway.
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