Extracorporeal Shockwave Therapy Alleviates Inflammatory Pain by Down-Regulating NLRP3 Inflammasome in Experimental Chronic Prostatitis and Chronic Pelvic Pain Syndrome
Purpose: To evaluate the anti-inflammatory and antioxidative effects of extracorporeal shockwave therapy (ESWT) on prostatitis and explore the mechanism of alleviating pain. Materials and Methods: For in vitro testing, RWPE-1 cells were randomly divided into 5 groups: (1) RWPE-1 group (normal con...
Main Authors: | , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
Published: |
Korean Society for Sexual Medicine and Andrology
2024-01-01
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Series: | The World Journal of Men's Health |
Subjects: |
Summary: | Purpose: To evaluate the anti-inflammatory and antioxidative effects of extracorporeal shockwave therapy (ESWT) on prostatitis
and explore the mechanism of alleviating pain.
Materials and Methods: For in vitro testing, RWPE-1 cells were randomly divided into 5 groups: (1) RWPE-1 group (normal
control), (2) LPS group (lipopolysaccharide inducing inflammation), (3) 0.1ESWT group (treated by 0.1 mJ/mm2 energy level),
(4) 0.2ESWT group (treated by 0.2 mJ/mm2 energy level), and (5) 0.3ESWT group (treated by 0.3 mJ/mm2 energy level). After
ESWT was administered, cells and supernatant were collected for ELISA and western blot. For in vivo testing, Sprague-
Dawley male rats were randomly divided into 3 groups: (1) normal group, (2) prostatitis group, and (3) ESWT group (n=12 for
each). Prostatitis was induced by 17 beta-estradiol and dihydrotestosterone (DHT) administration. Four weeks after ESWT, the
pain index was assessed for all groups and prostate tissues were collected for immunohistochemistry, immunofluorescence,
apoptosis analysis and, western blot.
Results: Our in vitro studies showed that the optimal energy flux density of ESWT was 0.2 mJ/mm2. In vivo, ESWT ameliorated
discomfort in rats with prostatitis and inflammation symptoms were improved. Compared to normal rats, overexpressed
NLRP3 inflammasomes triggered apoptosis in rats with prostatitis and this was improved by ESWT. TLR4-NFκB pathway was
overactive after experimental prostatitis, compared to normal and ESWT groups, and prostatitis induced alterations in BAX/
BAK pathway were inhibited by ESWT.
Conclusions: ESWT improved CP/CPPS by reducing NLRP3 inflammasome and ameliorated apoptosis via inhibiting BAX/
BAK pathway in a rat model. TLR4 may play a key role in bonding NLRP3 inflammasome and BAX/BAK pathways. ESWT
might be a promising approach for the treatment of CP/CPPS. |
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ISSN: | 2287-4208 2287-4690 |