Evaluation of receptor-interacting protein kinases (RIP1 and RIP3) in the therapeutic effect of thymoquinone against rat testis ischemia/reperfusion.

Torsion-induced ischemia causes lipid peroxidation in tissue, increases membrane permeability, and induces irreversible necroptosis in cells. The aim was to investigate the effects of thymoquinone (THQ) on receptor-interacting serine-threonine kinases (RIP1 and RIP3) after testicular torsion-induced ischemia/reperfusion (I/R). Control, ischemia/reperfusion (I/R), thymoquinone (THQ) 10 mg/kg and ischemia/reperfusion + thymoquinone (I/R+THQ). At the end of the experiment, spermiogram, histological and immunohistochemical, gene expression and biochemical analyses were performed on testicular tissue by collecting blood samples. Motility, testicular tissue seminiferous tubule epithelium thickness, tubule diameter and JTBS decreased in the I/R group compared to the Control and THQ groups.Both gene expression and immunoreactivity intensities of RIP1 and RIP3 increased in I/R. Furthermore, glial cell-derived neurotrophic factor (GDNF) and androgen-binding protein (ABP) decreased, steroidogenic acute regulatory protein (StAR), blood testosterone, and luteinizing hormone (LH) increased, and follicle-stimulating hormone (FSH) remained unchanged. THQ had a regulatory effect on all parameters. In addition to histopathological findings in testicular tissue, changes in RIP1, RIP3, GDNF, and StAR expression after I/R caused damage to both spermatogenic and non-spermatogenic tissue cell lines. Furthermore, changes in hormone levels indicate tissue dysfunction. The results reveal novel findings suggesting that THQ, applied after I/R, may be an effective compound for improving the structural and functional integrity of tissue; however, these findings need to be confirmed using various techniques with different application times and doses.