Emodin protects against apoptosis and inflammation by regulating reactive oxygen species-mediated NF-κB signaling in interleukin‐1β-stimulated human nucleus pulposus cells

Abstract

Intervertebral disc degeneration (IDD) is a complex degradative disorder associated with inflammation. Emodin, an anthraquinone derivative, possesses strong anti-inflammatory activity. This study focused on the in vitro therapeutic action of emodin in a cellular model of IDD. Human nucleus pulposus cells (NPCs) were stimulated with interleukin‐1 β (IL-1 β) to induce inflammation. Cell Counting Kit-8 and terminal deoxynucleotidyl transferase dUTP nick end labeling staining assays were performed to evaluate the viability and apoptosis of NPCs, respectively. Caspase-3 activity was measured to indirectly assess cell apoptosis. Western blot analysis was performed to detect protein expression levels. Reverse transcription‐polymerase chain reaction was performed for the detection of relative mRNA levels of tumor necrosis factor- α (TNF- α) and IL-6. Enzyme-linked immunosorbent assay was performed to analyze TNF- α and IL-6 secretion. Our results showed that emodin treatment mitigated IL-1β-induced reduction of cell viability in NPCs. Moreover, the increase in reactive oxygen species (ROS) production, apoptotic rate, and caspase-3 activity in IL-1 β-stimulated NPCs was reduced by emodin treatment. Treatment with emodin also abolished IL-1 β-induced inflammation in NPCs, as indicated by reduced secretion of IL-6 and TNF- α. Besides, the increase in expression levels of phosphorylated p65 and nuclear p65 in IL-1 β-stimulated NPCs was suppressed by emodin treatment. Furthermore, inhibition of nuclear factor kappa B (NF- κB) activation with pyrrolidine dithiocarbamate aggravated the protective effects of emodin. These results suggested that emodin protected NPCs against IL-1 β-induced apoptosis and inflammation via inhibiting ROS-mediated activation of NF- κB.

Qualitative and quantitative analysis methods for quality control of rhubarb in Taiwan’s markets

“…According to our result in the KEGG pathway, anthraquinones in rhubarb, including aloe-emodin, emodin, rhein, chrysophanol, and physcion, significantly affected the NF-kappa B signaling pathway—a prototypical pro-inflammatory signaling pathway implicated in chemical carcinogenesis. Emodin, an important anthraquinone with strong anti-inflammatory properties, protects human nucleus pulposus cells against IL-1 beta-induced apoptosis and inflammation via inhibiting ROS-mediated activation of NF-kappa B ( Zhu et al, 2023 ). Emodin also suppresses tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), iNOS, and COX-2 expression, and inhibits LPS-induced NF-kappa B activation, IKB alpha degradation, phosphorylation of ERK, JNK, and P38 ( Yang et al, 2014 ).…”

Ginsenoside Rg1 relieves rat intervertebral disc degeneration and inhibits IL-1β-induced nucleus pulposus cell apoptosis and inflammation via NF-κB signaling pathway

“…Emodin also was proved to protect NP cells against IL-1β-induced apoptosis and inflammation via inhibiting ROS-mediated activation of NF-κB pathway (Zhu et al . 2023 ). Ginsenoside Rg1 had been proved to promote growth and ECM synthesis of degenerative NP cells, delaying its degeneration (Lu et al .…”

Sinomenine Ameliorates IL-1β-Induced Intervertebral Disc Degeneration in Rats Through Suppressing Inflammation and Oxidative Stress via Keap1/Nrf2/NF-κB Signaling Pathways

“…It is well-established that IL-1β can activate the NF-κB signaling pathway, thereby promoting the synthesis of downstream inflammatory factors. 18 Consequently, IL-1β is frequently employed as an inflammatory inducer to establish a pro-inflammatory milieu within cells and tissues. This also accounts for the marked increase in IL-1β, IL-6, IL-17 and TNF-α synthesis observed following treatment with this cytokine in NPCs.…”