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Updated: May 25, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
[Apigenin regulates lipopolysaccharides-induced activation of inflammasome]
Ling-Yan Wang1, Jie Kuang, Jing Li
1Department of Dermatology, Jishuitan Hospital, Beijing 100035, China.
Objective:
To evaluate whether or not apigenin regulates the activation of inflammasome and elucidate its underlying mechanism.
Methods:
Cultured THP-1 (acute monocytic leukemia cell line) cells were treated with dimethyl sulfoxide (DMSO) alone (control group), lipopolysaccharides (LPS), LPS plus apigenin (25/50 µmol/L) or LPS plus Z-VAD (a caspase inhibitor). The supernatant was harvested and the content of secreted interleukin (IL)-1β was determined by enzyme-linked immunosorbent assay (ELISA). The effects of apigenin on the cleavage of pro-IL-1β and pro-caspase-1 were determined by Western blot. And the effect of apigenin on the nuclear factor (NF)-κB activation was detected by reporter gene assay.
Results:
MTT assays showed that the cytotoxicity of apigenin was low. Apigenin could significantly inhibit the LPS-induced secretion of IL-1β in THP-1 cells. The concentration of IL-1β was (362 ± 64) pg/ml in the control group, (1549 ± 320) pg/ml in the LPS group, (397 ± 150) pg/ml in the LPS plus 25 µmol/L apigenin group and (268 ± 142) pg/ml in the LPS plus 50 µmol/L apigenin group (P < 0.05). The results of Western blot indicated that apigenin inhibited the maturation of pro-IL-1β and pro-caspase-1. It could also inhibit the LPS-induced activation of NF-κB. The value of relative light unit was 0.6 ± 0.1 in the control group, 32.7 ± 0.8 in the LPS group, 12.9 ± 1.8 in the LPS plus 25 µmol/L apigenin group and 10.0 ± 3.2 in the LPS plus 50 µmol/L apigenin group respectively (P < 0.05).
Conclusion:
Apigenin may inhibit the LPS-induced activation of inflammasome through an inhibited muturation of caspase-1.
Insights
Apigenin, a natural compound, effectively inhibits inflammasome activation by reducing the maturation of caspase-1. This study demonstrates apigenin
Area of Science:
- Immunology
- Molecular Biology
- Pharmacology
Background:
- The inflammasome is a key regulator of inflammatory responses.
- Dysregulation of inflammasome activation is implicated in various diseases.
- Apigenin is a natural flavonoid with potential anti-inflammatory properties.
Purpose of the Study:
- To investigate the effect of apigenin on inflammasome activation.
- To elucidate the underlying molecular mechanisms of apigenin's action.
Main Methods:
- THP-1 cells were treated with lipopolysaccharides (LPS) and varying concentrations of apigenin.
- Interleukin (IL)-1β secretion was measured using ELISA.
- Western blot was employed to assess the cleavage of pro-IL-1β and pro-caspase-1.
- Reporter gene assay was used to detect nuclear factor (NF)-κB activation.
Main Results:
- Apigenin exhibited low cytotoxicity in THP-1 cells.
- Apigenin significantly inhibited LPS-induced IL-1β secretion.
- Apigenin suppressed the maturation of pro-IL-1β and pro-caspase-1.
- Apigenin attenuated LPS-induced NF-κB activation.
Conclusions:
- Apigenin inhibits LPS-induced inflammasome activation.
- The mechanism involves the inhibition of caspase-1 maturation.
- Apigenin demonstrates potential as a therapeutic agent for inflammatory conditions.
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