| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2023-03-10 |
| タイトル |
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|
タイトル |
Pathological analysis of spermatic dysfunction following testicular ischemia-reperfusion injury\n |
|
言語 |
en |
| 言語 |
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|
言語 |
eng |
| 資源タイプ |
|
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| 著者 |
HIRATA, Keita
OHIRA, Shin
TONE, Shigenobu
KAKUMAE, Sho
NAKATSUKA, Tota
MORINAKA, Hirofumi
TAKASAKI, Hiroyasu
SHIMIZU, Shinjiro
NAGAI, Atsushi
UEHARA, Shinya
|
| 著者所属(英) |
|
|
言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
|
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言語 |
en |
|
値 |
Faculty of Science and Engineering, Tokyo Denki University |
| 著者所属(英) |
|
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| 著者所属(英) |
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言語 |
en |
|
値 |
Director of Kawasaki Medical School Hospital |
| 著者所属(英) |
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言語 |
en |
|
値 |
Department of Urology, Kawasaki Medical School |
| キーワード |
|
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言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Testicular ischemia-reperfusion injury |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Spermatic dysfunction |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Pathological analysis |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Oxidative stress |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Inflammation\n |
| 抄録(英) |
|
|
言語 |
en |
|
値 |
Introduction & Objectives: Torsion, which may result in testicular ischemia, requires emergency surgery to restore testicular blood flow. However, the risk of spermatic dysfunction remains even if surgery is performed. The pathology of spermatic dysfunction in testicular ischemia-reperfusion injury (TIRI) remains unclear. A previous study showed the relevance of inflammation and oxidative stress in the other organs of ischemia-reperfusion injury. We hypothesized that inflammation and oxidative stress play key roles in causing spermatic dysfunction following TIRI. We investigated the pathophysiology of spermatic dysfunction in TIRI focusing on inflammatory changes using TIRI model mice.
Materials and Methods: The study used C57BL/6J male mice aged 10 to 15 weeks. To create TIRI model mice, the unilateral (left side) testicular vessels were clamped using Dieffenbach clamps (Bulldog clamps) for 1 hour and de-clamped. The bilateral testes were removed at 0 (ischemic state), 1, 3, and 5 weeks after creating the TIRI model mice. Spermatic changes following TIRI were investigated by analyzing the histology of the testes and semen and assessing levels of inflammation and oxidative stress. Semen was collected from the bilateral cauda epididymites and investigated using the sperm motility analysis system (SMAS).
Results: Histological analysis after hematoxylin-eosin staining showed tissue thickening in interstitial tissues at week 1 and 3 on the left (affected) testis, and week 1, 3 and 5 on the right (unaffected) testis. The infiltration of lymphocytes-predominant inflammatory cells were observed at week 1 and week 3 on the left (affected) testis. The destruction of ductal structures and giant cells were observed at weeks 3 and 5 on the left (affected) testis and week 5 on the right (unaffected) testis. SMAS showed significantly decreased spermatic concentration and motility in both testes of TIRI model mice compared with those of sham-operated mice at weeks 1, 3 and 5. Inflammation analysis using an inflammation-related proteome assay showed significantly increased levels of cytokines (IL-2, IL-3, IL-17A, and IL-23) and chemokines (CCL2, CCL5, CXCL1, and CX3CL1) at weeks 1, 3, and 5 in both testes of TIRI model mice. For the assessment of oxidative stress, enzyme-linked immuno-sorbent assay (ELISA) for 8-hydroxy-2’-deoxyguanosine (8-OHdG) was performed, which showed that levels of 8-OHdG were significantly increased in the left (affected) testis of TIRI model mice compared with that of sham-operated mice at all observation periods. Meanwhile, ELISA showed that levels of 8-OHdG in the right (unaffected) testis were significantly increased in TIRI model mice at weeks 3 and 5 compared with that of sham-operated mice.
Conclusions: Spermatic dysfunction following TIRI is induced by inflammation and oxidative stress. Inflammation and oxidative stress may be novel regulatory factors to prevent spermatic dysfunction following TIRI. |
| 書誌情報 |
en : Kawasaki medical journal
巻 48,
p. 131-140,
発行日 2022
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| 出版者 |
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出版者 |
Kawasaki Medical Society |
| ISSN |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
24343404 |
| 書誌レコードID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA12029005 |
| DOI |
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関連タイプ |
isIdenticalTo |
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|
識別子タイプ |
DOI |
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|
関連識別子 |
https://doi.org/10.11482/KMJ-E202248131 |
| 記事種別(英) |
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内容記述 |
Regular Article |
|
言語 |
en |
| 関連サイト |
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|
識別子タイプ |
URI |
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|
関連識別子 |
https://igakkai.kms-igakkai.com/wp/wp-content/uploads/2022en/KMJ-E202248131.pdf |
| 著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
PDF (3.2 MB)
