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Artemisinin ameliorates experimental autoimmune prostatitis by suppressing NLRP3 inflammasome-induced pyroptosis via
Rui Feng1, Andong Zhang2, Yiming Li3
1Urology Centre, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; Surgical Institute of Integrative Medicine, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; Surgical Institute, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; Shanghai Key Laboratory of Traditional Chinese Clinical Medicine, Shanghai 201203, China.
Abstract:
Chronic prostatitis (CP) is common in young males. The etiology is unclear and treatment options are limited. Pyroptosis, a newly identified type of cell death, has been linked to CP pathogenesis, warranting further investigation. Here, the therapeutic effects of artemisinin (ART) on chronic non-specific inflammation were assessed. Comprehensive analyses, including evaluation of chronic pain progression, histopathology, and cytokine levels, revealed that ART significantly and dose-dependently suppressed NOD-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptosis and alleviated pathological damage in experimental autoimmune prostatitis. Mechanistic studies indicated that ART markedly reduced oxidative stress in autoimmune mouse models by stimulating the Nrf2/HO-1 axis. The effects of ART were blocked by a specific Nrf2/HO-1 inhibitor, preventing inflammasome-mediated induction of pyroptosis. Cellular experiments showed that ART elevated Nrf2 levels and suppressed NLRP3 inflammasome-mediated pyroptosis in RAW264.7 macrophages following lipopolysaccharide (LPS) stimulation. In summary, ART mitigates CP by modulating the Nrf2/HO-1 pathway, thereby reducing oxidative stress and suppressing NLRP3-inflammasome-induced pyroptosis.
Insights
Artemisinin (ART) effectively treats chronic prostatitis (CP) by reducing inflammation and cell death. ART works by targeting the NLRP3 inflammasome pathway and reducing oxidative stress via the Nrf2/HO-1 axis.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Chronic prostatitis (CP) is a prevalent condition in young males with unclear causes and limited treatments.
- Pyroptosis, a form of programmed cell death, is implicated in the pathogenesis of CP.
- NOD-like receptor protein 3 (NLRP3) inflammasome activation and subsequent pyroptosis are key contributors to CP pathology.
Purpose of the Study:
- To investigate the therapeutic potential of artemisinin (ART) in treating chronic non-specific inflammation associated with CP.
- To elucidate the mechanisms by which ART exerts its anti-inflammatory and protective effects in experimental autoimmune prostatitis.
- To assess the role of the Nrf2/HO-1 pathway and NLRP3 inflammasome in ART's therapeutic action.
Main Methods:
- Experimental autoimmune prostatitis mouse models were used to evaluate ART's effects on chronic pain, histopathology, and cytokine levels.
- Mechanistic studies involved assessing oxidative stress markers and the activation of the Nrf2/HO-1 axis.
- In vitro experiments using RAW264.7 macrophages stimulated with lipopolysaccharide (LPS) were conducted to confirm ART's cellular effects.
Main Results:
- Artemisinin (ART) demonstrated significant, dose-dependent suppression of NLRP3 inflammasome-mediated pyroptosis and alleviated pathological damage in experimental autoimmune prostatitis.
- ART markedly reduced oxidative stress in mouse models by stimulating the Nrf2/HO-1 signaling pathway.
- ART treatment elevated Nrf2 levels and inhibited LPS-induced NLRP3 inflammasome-mediated pyroptosis in macrophages.
Conclusions:
- Artemisinin (ART) mitigates chronic prostatitis (CP) by modulating the Nrf2/HO-1 pathway, thereby reducing oxidative stress.
- ART effectively suppresses NLRP3 inflammasome-induced pyroptosis, offering a potential therapeutic strategy for CP.
- Targeting the Nrf2/HO-1 axis and NLRP3 inflammasome represents a promising approach for managing chronic prostatitis.