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Objectives: In this study, we aimed to investigate the therapeutic effects of magnesium sulfate (MgSO4) and dexmedetomidine (dex) in a model of acute lung injury (ALI). We determined whether concomitant administration decreased the inflammatory effects of hydrochloric acid (HCl)-induced ALI in a synergistic manner. Materials and Methods: In this study, 42 Sprague–Dawley rats were randomized into six groups: Group S (saline), Group SV (saline + mechanical ventilation), Group HCl (HCl), Group Dex (Dex), Group Mag (MgSO4), and Group DM (Dex + MgSO4). All groups except Group S were mechanically ventilated prior to HCl-induced ALI. Saline or HCl was administered via tracheostomy. Prior to treatment, HCl was administered to Group HCl, Group Dex, Group Mag, and Group DM to induce ALI. Dex and MgSO4 were administered intraperitoneally. The rats were monitored for 4 h after treatment to measure oxidative stress parameters in blood, and prolidase enzyme activity. Lung tissue damage were determined via histopathology. Results: A significant increase in heart rate and rapid desaturation was observed in HCl-administered groups. Treatment administration decreased the pulse values. Increased saturation values and decreased oxidative stress indices were observed in groups that were subsequently administered​ Dex and MgSO4. Serum prolidase activity increased significantly in Group HCl. Severe pathological findings were detected following HCl-induced ALI. Group Mag showed greater improvement in the pathology of HCl-induced ALI than did Group Dex. Administration of both Dex and MgSO4 did not improve the pathological scores. Conclusions: The antioxidant and anti-inflammatory effects of Dex and MgSO4 ameliorated the detrimental effects of HCI-induced ALI. However, adverse effects on hemodynamics and lung damage were observed when the two drugs were administered together.

Objective: To investigate the role of cordycepin in testicular ischemia/reperfusion injury in rats. Materials and methods: Forty Wistar albino rats were randomly divided into four groups, as follows: group one, control (C); group two, torsion and ischemia (I); group three: detorsion with ischemia–reperfusion (IR); and group four, detorsion/cordycepin. The rats were then analyzed macromorphologically and histopathologically, and blood tests were performed. Specifically, the total oxidant status (TOS) and total antioxidant status (TAS) were determined, and malondialdehyde (MDA), tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β levels were analyzed. In addition, pyknotic nuclei, spermatozoa, edema, and hemorrhage were assessed. Results: When the IR and cordycepin groups were compared with the other groups, there was a statistically significant decrease in TNF-α and MDA levels (p < 0.05). Increased TAS levels were observed in the cordycepin group compared with the control group. TOS levels were significantly increased in the I and IR groups, but decreased in the cordycepin group (p < 0.05). Similar effects were observed in tissue biochemistry analysis. Histopathological evaluations revealed that the spermatozoa count was decreased in the I and IR groups. However, there was an increase in the cordycepin group, as well as a statistically significant difference between the IR and cordycepin groups (p < 0.01). Finally, edema and inflammation were increased in the I and IR groups, but decreased in the cordycepin group. Conclusions: Histological and biochemical findings revealed that cordycepin protected against IR-induced testicular injury.