{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T23:46:09Z","timestamp":1790984769962,"version":"4.1.0"},"reference-count":32,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,3]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Experimental autoimmune prostatitis (EAP)-induced persistent inflammatory immune response can significantly upregulate the expression of N-methyl-D-aspartic acid (NMDA) receptors in the paraventricular nucleus (PVN). However, the mechanism has not yet been elucidated. Herein, we screened out the target prostate-derived inflammation cytokines (PDICs) by comparing the inflammatory cytokine levels in peripheral blood and cerebrospinal fluid (CSF) between EAP rats and their controls. After identifying the target PDIC, qualified males in initial copulatory behavior testing (CBT) were subjected to implanting tubes onto bilateral PVN. Next, they were randomly divided into four subgroups (EAP-1, EAP-2, Control-1, and Control-2). After 1-week recovery, EAP-1 rats were microinjected with the target PDIC inhibitor, Control-1 rats were microinjected with the target PDIC, while the EAP-2 and Control-2 subgroups were only treated with the same amount of artificial CSF (aCSF). Results showed that only interleukin-1\u03b2 (IL-1\u03b2) had significantly increased mRNA-expression in the prostate of EAP rats compared to the controls (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.001) and significantly higher protein concentrations in both the serum (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.001) and CSF (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.001) of the EAP groups compared to the Control groups. Therefore, IL-1\u03b2 was identified as the target PDIC which crosses the blood-brain barrier, thereby influencing the central nervous system. Moreover, the EAP-1 subgroup displayed a gradually prolonged ejaculation latency (EL) in the last three CBTs (all\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.01) and a significantly lower expression of NMDA NR1 subunit in the PVN (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.043) compared to the respective control groups after a 10-day central administration of IL-1\u03b2 inhibitors. However, the Control-1 subgroup showed a gradually shortened EL (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.01) and a significantly higher NR1 expression (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.004) after homochronous IL-1\u03b2 administration. Therefore, we identified IL-1\u03b2 as the primary PDIC which shortens EL in EAP rats. However, further studies should be conducted to elucidate the specific molecular mechanisms through which IL-1\u03b2 upregulates NMDA expression.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/aja202142","type":"journal-article","created":{"date-parts":[[2021,8,13]],"date-time":"2021-08-13T11:26:05Z","timestamp":1628853965000},"page":"213-218","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":5,"title":["Prostate-derived IL-1\u03b2 upregulates expression of NMDA receptor in the paraventricular nucleus and shortens ejaculation latency in rats with experimental autoimmune prostatitis"],"prefix":"10.4103","volume":"24","author":[{"given":"Jie","family":"Yang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiao-Chen","family":"Luan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian-Huai","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qi-Jie","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian-Xin","family":"Xue","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ya-Min","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo-Qing","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning-Hong","family":"Song","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zeng-Jun","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia-Dong","family":"Xia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-17-20240829","doi-asserted-by":"crossref","first-page":"1009","DOI":"10.1007\/s00345-015-1720-3","article-title":"Prevalence 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