Studies have shown that ischemia-reperfusion (I/R) produces free radicals leading to lipid peroxidation and to damage of the nervous tissue. Melatonin, a main secretory product of the pineal gland, has free radical scavenging and antioxidant properties and has been shown to diminish I/R injury in many tissues. There are a limited number of studies related to the effects of melatonin on I/R injury in the peripheral nervous system. Therefore, in the present study, the protective effect of melatonin was investigated in rats subjected to 2 hr of sciatic nerve ischemia followed by 3 hr of reperfusion. Following reperfusion, nerve tissue samples were collected for quantitative assessment of malondialdehyde (MDA), an oxidative stress marker, and superoxide dismutase (SOD), a principal antioxidant enzyme. Samples were further evaluated at electron microscopic level to examine the neuropathological changes. I/R elevated the concentration of MDA significantly while there was a reduction at SOD levels. Melatonin treatment reversed the I/R-induced increase and decrease in MDA and SOD levels, respectively. Furthermore, melatonin salvaged the nerve fibers from ischemic degeneration. Histopathologic findings in the samples of melatonin-treated animals indicated less edema and less damage to the myelin sheaths and axons than those observed in the control samples. Our results suggest that administration of melatonin protects the sciatic nerve from I/R injury, which may be attributed to its antioxidant property.

AimThe aim of this study was to investigate the effects of levosimendan and thymoquinone (TQ) on lung injury after myocardial ischemia/reperfusion (I/R).Materials and methodsTwenty-four Wistar albino rats were included in the study. The animals were randomly assigned to 1 of 4 experimental groups. In Group C (control group), left anterior descending artery was not occluded or reperfused. Myocardial I/R was induced by ligation of the left anterior descending artery for 30 min, followed by 2 h of reperfusion in the I/R, I/R-levosimendan (24 µg/kg) (IRL) group, and I/R-thymoquinone (0.2 mL/kg) (IRTQ) group. Tissue samples taken from the lungs of rats were histochemically stained with H&E and immunohistochemically stained with p53, Bcl 2, Bax, and caspase 3 primer antibodies.ResultsIncreased expression of p53 and Bax was observed (4+), especially in the I/R group. In IRTQ and IRL groups, expression was also observed at various locations (2+, 3+). H&E staining revealed that that the lungs were severely damaged and the walls of the alveoli were too thick, the number of areas examined was increased during the evaluation. Caspase 3 expression was observed to be at an (1+, 2+) intensity that was usually weak and diffuse in multiple areas. Bcl 2 was not found to be expressed in any of the tissues. H&E staining revealed that that the lungs were severely damaged in the I/R group, with the walls of the channels and alveoli thickened and edematous, and also an intense inflammatory cell migration was observed. Immunohistochemical staining was more prominent in inflammatory areas and structures around the terminal bronchioles.ConclusionThe findings in our study have shown that administration of levosimendan and TQ during I/R increases expression of caspase 3, p53, and Bax in lung tissue and has a protective effect on lung as distant organ. We suggest that findings of this study be elucidated with further large-scale clinical studies.

Aim: The aim of this study was to investigate whether dexmedetomidine – administered before ischemia – has protective effects against lower extremity ischemia reperfusion injury that induced by clamping and subsequent declamping of infra-renal abdominal aorta in streptozotocin-induced diabetic rats. Material and Methods: After obtaining ethical committee approval, four study groups each containing six rats were created (Control (Group C), diabetes-control (Group DM-C), diabetes I/R (Group DM-I/R), and diabetes-I/R-dexmedetomidine (Group DM-I/R-D). In diabetes groups, single-dose (55 mg/kg) streptozotocin was administered intraperitoneally. Rats with a blood glucose level above 250 mg/dl at the 72nd hour were accepted as diabetic. At the end of four weeks, laparotomy was performed in all rats. Nothing else was done in Group C and DM-C. In Group DM-I/R, ischemia reperfusion was produced via two-hour periods of clamping and subsequent declamping of infra-renal abdominal aorta. In Group DM-I/R-D, 100 μg/kg dexmedetomidine was administered intraperitoneally 30 minutes before ischemia period. At the end of reperfusion, period biochemical and histopathological evaluation of renal tissue specimen were performed. Results: Thiobarbituric acid reactive substance (TBARS), Superoxide dismutase (SOD), Nitric oxide synthase (NOS), Catalase (CAT) and Glutathion S transferase (GST) levels were found significantly higher in Group DM-I/R when compared with Group C and Group DM-C. In the dexmedetomidine-treated group, TBARS, NOS, CAT, and GST levels were significantly lower than those measured in the Group D-I/R. In histopathological evaluation, glomerular vacuolization (GV), tubular dilatation (TD), vascular vacuolization and hypertrophy (VVH), tubular cell degeneration and necrosis (TCDN), tubular hyaline cylinder (THC), leucocyte infiltration (LI), and tubular cell spillage (TCS) in Group DM-I/R were significantly increased when compared with the control group. Also, GV, VVH, and THC levels in the dexmedetomidine-treated group (Group DM-I/R-D) were found significantly decreased when compared with the Group DM-I/R. Conclusion: We found that dexmedetomidine − 100 μg/kg intraperitoneally – administered 30 minutes before ischemia in diabetic rats ameliorates lipid peroxidation, oxidative stress, and I-R-related renal injury. We suggest that dexmedetomidine administration in diabetic rats before I/R has renoprotective effects.

Introduction: We aimed to investigate the effects of cerium oxide, applied before the sevoflurane anesthesia, on lung tissue in rats with lower extremity ischemia-reperfusion (IR). Materials and Methods: A total of 30 rats were randomly divided into five groups as; control (C), IR, cerium oxide-IR (CO-IR), IR-sevoflurane (IRS), and cerium oxide-IRsevoflurane (CO-IRS). In the CO-IR group, 30 minutes after the injection of cerium oxide (0.5 mg/kg, intraperitoneal (i.p)), an atraumatic microvascular clamp was placed on the infrarenal abdominal aorta for 120 minutes. Then, the clamp was removed and reperfused for 120 minutes. Sevoflurane was applied in 100% oxygen at a rate of 2.3% at 4 L/min during IR. The blood samples were taken for biochemical analysis and the lung tissue samples were taken for histological analysis. Results: Neutrophil infiltration/aggregation was significantly higher in the IR group than in the C and CO-IRS groups. The alveolar wall thickness and total lung injury scores were significantly higher in the IR group than in the C, IRS, CO-IR and CO-IRS groups. Discussion: We determined that the administration of 0.5 mg/kg dose of cerium oxide with sevoflurane reduces the oxidative stress and corrects IR-related damage in lung tissue. Our results show that the administration of cerium oxide before IR and the administration of sevoflurane during IR have a protective effect in rats.

The aim of this study is to demonstrate whether fullerenol C60 protects renal injury in sevofl urane-administered rats. METHOD: Rats (n: 24) were randomly divided into four groups: Control (Group C), Fullerenol C60 (Group F), Sevofl urane (Group S), Fullerenol C60-Sevofl urane (Group FS). Thirty minutes before the procedure, Fullerenol C60, 100 mg/kg, was administered intraperitoneally. Sevofl urane (2.3 %) was applied for 3 hours to rats in S and FS groups. Biochemical and histopathological parameters were analyzed in renal tissue samples. Kruskal-Wallis and Mann-Whitney U tests were used in statistical analyzes. RESULTS: Malondialdehyde (MDA) level and catalase (CAT) enzyme activity in Group S were signifi cantly higher than that in all other groups. Paraoxanase (PON) enzyme activity in Group S was signifi cantly lower than in Groups C and FS. The histopathological examination showed that vascular vacuolization and hypertrophy (VVH) and lymphocyte infi ltration (LI) were signifi cantly higher in the Group S compared to the Group C. CONCLUSION: Renal histopathology revealed that the administration of Fullerenol C60 prior to sevofl urane inhalation reduced oxidative stress and partially corrected the damage caused by anesthesia. We concluded that Fullerenol C60 has a renal protective effect in rats when administered before sevofl urane anesthesia (Tab. 2, Fig. 4, Ref. 40).