Kisspeptin–1 (KISS–1) and Spexin (SPX) are neuropeptides that play crucial roles in metabolism and sexual function, with their expression levels in tissues potentially influenced by antioxidant treatments. This study aimed to investigate the effects of cortexin treatment against ischemia–reperfusion injury (I/R) resulting from testicular torsion on KISS–1 and SPX levels in testicular tissues. Twenty–eight male Sprague–Dawley, rats, aged 8–10 weeks, were divided into four equal groups: control, torsion, torsion/ detorsion, and torsion/detorsion+cortexin. At the conclusion of the experiment, histopathological and immunohistochemical analyses were performed to assess the expressions of KISS–1, SPX, tumor necrosis factor–alpha (TNF–α), and Caspase–3 in the testicular tissues. For biochemical analyses, total antioxidant status (TAS) and total oxidant status (TOS) levels were measured in serum samples using the ELISA method, while malondialdehyde (MDA) levels were assessed spectrophotometrically in testicular tissues. The results showed that compared to the control group, the torsion and torsion/detorsion groups exhibited significant histopathological damage, along with increased levels of MDA, TOS, Caspase–3, and TNF–α, and decreased levels of TAS, KISS–1, and SPX in the testicular tissues. Conversely, in the torsion+detorsion+cortexin group, which received treatment for reperfusion injury, there was a notable reduction in tissue damage, with decreased levels of MDA, TOS, caspase–3, and TNF–α, alongside increased levels of TAS, KISS, and SPX. Cortexin decreases testicular damage by reducing oxidative stress, increases spermatogenesis by improving seminiferous tubule and germinal epithelial thickness, and regulates KISS–1 and SPX expression, which have effects on the reproductive system.

Cyclophosphamide (CP) is a common chemotherapeutic drug; however, it does have several toxic side effects, including cardiotoxicity. Beta (β)-glucan is a free radical scavenger and powerful antioxidative molecule. The effects of β-glucan on CP-induced cardiotoxicity were investigated in this experimental study. Twenty-eight Wistar albino rats were divided into the following four equal groups: control (no treatment), CP (200 mg/kg CP, intraperitoneally on day 2), β-glucan (50 mg/kg β-glucan, oral gavage for seven days), and CP+β-glucan (200 mg/kg CP, intraperitoneally on day 2+50 mg/kg β-glucan, oral gavage for seven days) groups. Histopathology, irisin, and caspase-3 expressions were evaluated in ventricular myocardial tissues. The CP group exhibited considerably more severe cardiac damage than the control group, according to histological evaluation. Immunohistochemically irisin expression was decreased, and caspase-3 expression was much higher in the CP group. β-glucan, on the other hand, improved histopathological changes and exhibited a protective potential against CP-induced cardiac tissue damage when combined with the CP group. Our findings showed that β-glucan could act as an effective cardioprotective molecule against the toxic effects caused by CP.

Background/Aim: Cyclophosphamide (CP) is an anti-cancer agent that mediates nephrotoxicity. Beta (β)-glucan has restorative effects on kidney toxicities through its antioxidant potential; however, the effects of β-glucan on CP-induced renal injury remain unknown. In an experimental nephrotoxicity model using rats, we sought to examine the potential protective action of β-glucan on kidney histomorphology, apoptosis, and TNF-α expression. Methods: Male albino Wistar rats were divided equally into four groups: control, CP, β-glucan, and CP+β-glucan. The kidney tissues of the rats were examined for TNF-α and caspase-3 immunostaining to evaluate inflammation and apoptosis, respectively. Hematoxylin and eosin (H&E) and periodic acid–Schiff (PAS) staining were used for histopathological analyses. Results: The CP group showed severe histopathological damage in the renal tissues of rats. In the renal tissue of the CP group, immunoreactivities for TNF-α (1.25 [0.079] and caspase-3 (1.506 [0.143] were also higher than the control group (0.117 [0.006] and 0.116 [0.002], respectively; P<0.001). In the CP+β-glucan group, the histopathological changes significantly improved. Conclusion: Beta-glucan has therapeutic potential against CP-induced nephrotoxicity in rat kidney.

Aim: Cisplatin (CP) is used to treat a variety of cancers as a chemotherapeutic agent. This drug has also severe side effects and its use exhibits serious toxicity in a number of organs, including kidney and heart. The aim of the present study was to evaluate the ultrastructural and inflammatory changes induced by CP treatment in rat cardiac tissue in a time-dependent manner. Material and Methods: Rats were randomly divided into three experimental groups; control (only saline), CP D2 (treated with CP 2.5 mg/kg/day for 2 days), and CP D7 (treated with CP 2.5 mg/kg/day for 7 days). Cardiac tissues were examined under an electron microscope. Inflammation markers including tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) were analyzed by immunohistochemistry. In addition, electrocardiography was performed to measure the electrical activity. Results: The ultrastructural analysis of the CP D7 group revealed that myofibrils were disrupted and disorganized, mitochondria degenerated, and interstitial edema developed. When compared to the control and CP D2 groups, there was a noticeable increase in the level of TNF-α and IL-1β expression in the CP D7 group according to immunohistochemistry results. Electrocardiography showed that RR interval was longer in CP D7 than CP D2 and control groups. Conclusion: CP for 7 days damaged the ultrastructural morphology in cardiac tissue. Therefore, these findings suggest that the potential therapeutic approaches to reduce mitochondrial damage and inflammation against toxicity caused by CP may provide for clinically significant prevention when using the drug for an extended period of time.