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Effects of prokineticin 2 on testicular inflammation in rats
Author(s) -
Li Ying,
Wang Jiaojiao,
Yu Lili,
Zhao Kai,
Chen Biao,
Li Cuiling,
Yang Fan,
Yuan Hongfang,
Zhang Huiping
Publication year - 2018
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12843
Subject(s) - downregulation and upregulation , inflammation , nitric oxide synthase , endocrinology , receptor , orchitis , medicine , biology , nitric oxide , apoptosis , immunology , gene , pathology , biochemistry
Problem Prokineticin 2 ( PK 2), a pro‐inflammatory peptide, is highly expressed in primary spermatocytes. However, systematic research on PK 2 and testicular inflammation is lacking to date. Method of study An experimental autoimmune orchitis ( EAO ) model was established to detect the expression of PK 2 and its receptor (prokineticin receptor 1, PKR 1) 50 and 80 days after immunization. PK 2 si RNA sequence was injected into the rat rete testis to downregulate the expression of PK 2. PK 2 was over‐expressed in the testis by injecting PK 2 protein through the rat rete testis at different concentrations. Testicular morphology and expression of inducible nitric oxide synthase ( iNOS ) were detected after the intervention. Results Results showed that PK 2 and PKR 1 were upregulated in EAO at 50 days and downregulated at 80 days. PK 2 over‐expression contributed to the apoptosis of spermatogenic epithelial cells and increased infiltration of the inflammatory cells, whereas PK 2 under‐expression showed no change. Furthermore, iNOS expression was increased significantly when PK 2 was over‐expressed. Conclusion This finding demonstrated that the PK 2/ PKR 1 signals may have an essential role in the regulation of testicular inflammation through iNOS . PK 2 interference may represent a novel and promising therapeutic strategy for the clinical management of orchitis.

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