The aim of this study was to investigate the oxidative damage and inflammatory effects in the hippocampus and cerebellum in lipopolysaccharide (LPS)-induced sepsis model and possible ameliorating effects of pregabalin (PG). Twenty four female Wistar Albino rats (12 month old) were divided into 3 groups as follows: Group I (Control; 0.1 ml/gavage and i.p. saline, single dose), Group II (LPS; 5 mg/kg LPS, i.p, single dose), Group III (LPS + PG; 5 mg/kg LPS, i.p, single dose + 30 mg/kg, gavage, single dose). DNA damage, ischemia-modified albumin (IMA), total oxidant status (TOS), total antioxidant status (TAS) oxidative stress index (OSI), leukocyte (WBC), lymphocyte, neutrophil, hemoglobin (HGB), erythrocyte (RBC), and thrombocyte counts were measured in blood and brain tissues. Histopathological and immunohistochemical evaluation of Caspase- 3, G-CSF, IL-6, SAA, iNOS expressions were conducted using hippocampus and cerebellum tissues. Comet analysis score, lymphocytes, neutrophils, WBC, IMA, TOS and OSI values were increased in Group II compared with to Group I (p < 0.05). IMA levels in blood, TOS and OSI levels in the brain were significantly decreased in Group III compared to Group II (p < 0.05). We observed increased hemorrhages, neutrophils, leukocytes infiltrations and neuron degeneration in Group II compared to Group I. Caspase 3, G-CSF, IL-6, SAA, iNOS expressions were increased in group II compared to Group I (p < 0.001). Pregabalin partly ameliorated the damage caused by the exposure to LPS in hippocampus and cerebellum; however, further studies are needed to determine pregabalin's possible protective effects at different doses and with different techniques.

High fructose corn syrup (HFCS) has been shown to cause cardiovascular toxicity via oxidative stress and inflammation. The aim of this study is to demonstrate the protective effects of melatonin (MLT) against HFCS-induced endothelial and cardiac dysfunction via oxidative stress and inflammation. Thirty-two Sprague Dawley male rats were distributed into three groups as control, HFCS, and HFCS + MLT. HFCS form F55 was prepared as 20% fructose syrup solution and given to the rats through drinking water for 10 weeks, and MLT administrated 10 mg/kg/day orally for last 6 weeks in addition to F55. After decapitation, blood and half of the heart samples were collected for biochemical analysis and other half of the tissues for histopathological and immunohistochemical analysis. Aspartate transaminase, creatine kinase MB, lactate dehydrogenase, total oxidant status and oxidative stress index, and caspase-3 levels increased and total antioxidant status levels decreased significantly in HFCS group. MLT treatment reversed all these parameters. Histopathologically, hyperemia, endothelial cell damage and increased levels of angiogenin, C-reactive protein, inducible nitric oxide synthase, myeloperoxidase and decreased sirtuin-1 (SIRT-1) expressions were observed in HFCS group. MLT ameliorated all these changes. MLT has an anti-inflammatory, antioxidant, antiapoptotic effects on HFCS-induced cardiovascular toxicity through enhancing the expression of SIRT-1.