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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

This study aimed to establish the relationship between two endoplasmic reticulum (ER) stress proteins, glucose-regulated protein 78 (GRP78/BiP) and PKR-like endoplasmic reticulum kinase (PERK), and oxidative stress markers in cisplatin (CIS)-induced and gentamicin (GEN)-induced nephrotoxicity.The study consisted of five groups: control (saline solution only), CIS D2 (2.5 mg/kg for 2 days), CIS D7 (2.5 mg/kg for 7 days), GEN D2 (160 mg/kg for 2 days), and GEN D7 (160 mg/kg for 7 days). All rats were sacrificed 24 h after the last injection for standard clinical chemistry, and ultrastructural and histological evaluation of the kidney.CIS and GEN increased blood urea nitrogen (BUN) and serum creatinine (Cr) levels, as well as total oxidant status (TOS), while decreasing total antioxidant status (TAS) level in CIS D7 and GEN D7 groups. Histopathological and ultrastructural findings were also consistent with renal tubular damage. In addition, expression of markers of renal inflammation (tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β)) and ER stress markers (GRP78 and PERK) was significantly increased in the kidney tissue of rats treated with CIS and GEN for 7 days.These findings suggest that CIS and GEN administration for 7 days aggravates nephrotoxicity through the enhancement of oxidative stress, inflammation, and ER stress-related markers. As a result, the recommended course of action is to utilize CIS and GEN as an immediate but brief induction therapy, stopping after 3 days and switching to other drugs instead.

Doxorubicin is an anthracycline chemotherapeutic agent that causes cardiomyopathy as a side effect. Here, we aimed to investigate the effects of linagliptin and bisoprolol on the management of doxorubicin-induced cardiomyopathy in rats. Wistar rats were divided into six groups (n = 8). Group I received saline for 4 weeks; group II received 1 mg/kg bisoprolol for 8 weeks; group III received 3 mg/kg linagliptin for 8 weeks; group IV received 1.25 mg/kg doxorubicin for 4 weeks for the induction of cardiomyopathy; group V received 1.25 mg/kg doxorubicin for 4 weeks plus 1 mg/kg bisoprolol for 8 weeks; and group VI received 1.25 mg/kg doxorubicin for 4 weeks plus 3 mg/kg linagliptin for 8 weeks. Electrocardiography and isometric mechanography were conducted to measure ventricular contractile responses. Myocardial tissue and serum samples were analyzed for oxidative and cardiotoxic markers by ELISA. Electrocardiography revealed that QRS, QT and Tp intervals were longer in group IV than group I. Doxorubicin caused a significant decrease in ventricular contraction, which was significantly prevented by bisoprolol. Doxorubicin resulted in myocardial fiber disorganization and disruption, but bisoprolol or linagliptin improved this myocardial damage. Glutathione peroxidase was significantly decreased in groups IV and V. Bisoprolol or linagliptin treatment attenuated the significant doxorubicin-mediated increase in malondialdehyde. Doxorubicin and linagliptin provided significant elevations in CK-MB activity and troponin-I levels. Doxorubicin resulted in pronounced oxidative stress. The beneficial effects of bisoprolol and linagliptin on myocardial functional, histopathological and biochemical changes could be related to the attenuation of oxidative load.

The management of chronic peripheral neuropathic pain conditions with conventional treatments is still limited. In this present study, we aimed to determine the anti-neuropathic actions of pulsed magnetic field (PMF) treatments as a therapeutic. Effects of daily PMF treatments for 4 weeks were investigated by examining pain behaviors, hyperalgesia and allodynia, electrophysiological parameters, amplitude of compound action potential (CAP) and sciatic nerve conduction velocity (SNCV) and histopathological changes in rats with chronic constriction injury (CCI). Peripheral and central pro-inflammatory cytokines (TNF alpha, IL-113 and IL-17), chemokines (CCL3 and CXCL1) and angiogenic factors (VEGF and bFGF) in sciatic nerves and spinal cord tissues were also measured for determining the possible molecular action mechanisms of PMF treatment. Hyperalgesia and allodynia were observed at the first week and lasted for 4 weeks after CCI. PMF treatments caused timedependent anti-hyperalgesic and anti-allodynic effects. PMF treatment alleviated the histopathological consequences of CCI on sciatic nerve and significantly improved the amplitude of the CAP and SNCV. PMF treatment inhibited the pro-inflammatory molecules and promoted the anti-inflammatory cytokines in neural tissues. PMF treatment also suppressed the VEGF levels and enhanced the bFGF levels in both neural tissues. The results of the present study suggested that daily PMF treatment may have neuroprotective and anti-neuropathic pain actions in rats with CCI-induced neuropathy due to its modulating effects on neuro-inflammatory and neuro-angiogenic mediators in central and peripheral neural tissues.

Objective: We aimed to investigate the protective effect of adrenomedullin (ADM) on cerebral tissue of rats with cerebral ischemia/reperfusion (I/R) injury. Methods: Thirty-two Wistar rats were randomized into four groups (n=8). In the I/R Group, bilateral common carotid arteries were clamped for 30 minutes and, subsequently, reperfused for 120 minutes. In the ADM Group, rats received 12 µg/kg of ADM. In the I/R+ADM Group, bilateral common carotid arteries were clamped for 30 minutes and, subsequently, the rats received 12 µg/ kg of ADM. Then, reperfusion was performed for 120 minutes. The Control Group underwent no procedure. Blood and brain tissue samples were collected for biochemical and histopathological analysis. Serum malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were analysed. Brain tissue was evaluated histopathologically and neuronal cells were counted in five different fields, at a magnification of ×400. Results: Brain MDA in I/R Group was significantly higher than in ADM Group. Brain GPx and SOD in I/R+ADM Group were significantly higher than in I/R Group. The number of neurons was decreased in I/R Group compared to the Control Group. The number of neurons in I/R+ADM Group was significantly higher than in I/R Group, and lower than in Control Group. Apoptotic changes decreased significantly in I/R+ADM Group and the cell structure was similar in morphology compared to the Control Group. Conclusion: We demonstrated the cerebral protective effect of ADM in the rat model of cerebral I/R injury after bilateral carotid artery occlusion.