Open AccessInvolvement of Asc and Nlrp3 inflammasomes in the testes following spinal cord injury
Author(s) -
Hajar Ramezanikhah,
Ahmad Farrokhi,
Reza Nejatbakhsh,
Saeed Shokri,
Adib Zendedel,
Alireza Abdanipour
Publication year - 2020
Publication title -
endocrine regulations
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.456
H-Index - 32
eISSN - 1336-0329
pISSN - 1210-0668
DOI - 10.2478/enr-2020-0012
Subject(s) - spermatogenesis , andrology , tunel assay , apoptosis , medicine , spinal cord injury , germ cell , endocrinology , spinal cord , biology , immunohistochemistry , biochemistry , psychiatry , gene
Objective. The exact mechanism, by which spinal cord injury (SCI) leads to a male subfertility is not well-known. Present study was conducted to determine the mechanisms that lead to the elevated end-product cytokines and inflammasomes in the testes of an SCI rat model. Moreover, we evaluated the inflammasome components following SCI in testis over a defined time periods. Methods. Weight drop technique was used to induce SCI at the level of the T10 vertebra in male Wistar rats. The animals were sacrificed at specific time intervals (3, 7, 14, 21, and 28 day’s post-SCI). mRNA levels of inflammasomes and cytokines were measured by real-time PCR, germ cells apoptosis was evaluated by TUNEL staining, and the epithelium of seminiferous tubules by Miller’s and Johnsen’s scores. Results. The results showed activation of Nlrp3 in the testes of SCI animals at different time points. Expression of Nlrp3 and IL-1β sharply increased 14 days after the SCI. Upregulation of IL-1β and IL-18 at days 14 and 21 post-SCI might disintegrate the epithelium of seminiferous tubules at day 14 and induce germ cells apoptosis, increase abnormal sperm cells, and attenuate motility and viability at 21 days post-SCI. Conclusion. This study provided further evidence of innate immunity activation in testes that could lead to more disruption of spermatogenesis in SCI patients at specific times.