Problem: Prokineticin 2 (PK2), a pro-inflammatory peptide, is highly expressed in primary spermatocytes. However, systematic research on PK2 and testicular inflammation is lacking to date.
Method of study: An experimental autoimmune orchitis (EAO) model was established to detect the expression of PK2 and its receptor (prokineticin receptor 1, PKR1) 50 and 80 days after immunization. PK2 siRNA sequence was injected into the rat rete testis to downregulate the expression of PK2. PK2 was over-expressed in the testis by injecting PK2 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 PK2 and PKR1 were upregulated in EAO at 50 days and downregulated at 80 days. PK2 over-expression contributed to the apoptosis of spermatogenic epithelial cells and increased infiltration of the inflammatory cells, whereas PK2 under-expression showed no change. Furthermore, iNOS expression was increased significantly when PK2 was over-expressed.
Conclusion: This finding demonstrated that the PK2/PKR1 signals may have an essential role in the regulation of testicular inflammation through iNOS. PK2 interference may represent a novel and promising therapeutic strategy for the clinical management of orchitis.
Keywords: inducible nitric oxide synthase; inflammation; male infertility; prokineticin 2.
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