BackgroundOxidative stress has a pivotal role in the pathogenesis and development of diabetic peripheral neuropathy (DPN), the most common and debilitating complications of diabetes mellitus. There is accumulating evidence that Juglans regia L. (GRL) leaf extract, a rich source of phenolic components, has hypoglycemic and antioxidative properties. This study aimed to determine the protective effects of Juglans regia L. leaf extract against streptozotocin-induced diabetic neuropathy in rat.MethodsThe DPN rat model was generated by intraperitoneal injection of a single 55 mg/kg dose of streptozotocin (STZ). A subset of the STZ-induced diabetic rats intragastically administered with GRL leaf extract (200 mg/kg/day) before or after the onset of neuropathy, whereas other diabetic rats received only isotonic saline as the same volume of GRL leaf extract. To evaluate the effects of GRL leaf extract on the diabetic neuropathy various parameters, including histopathology and immunohistochemistry of apoptotic and inflammatory factors were assessed along with nociceptive and biochemical assessments.ResultsDegeneration of the sciatic nerves which was detected in the STZ-diabetic rats attenuated after GRL leaf extract administration. Greater caspase-3, COX-2, and iNOS expression could be detected in the STZ-diabetic rats, which were significantly attenuated after GRL leaf extract administration. Also, attenuation of lipid peroxidation and nociceptive response along with improved antioxidant status in the sciatic nerve of diabetic rats were detected after GRL leaf extract administration. In other word, GRL leaf extract ameliorated the behavioral and structural indices of diabetic neuropathy even after the onset of neuropathy, in addition to blood sugar reduction.ConclusionOur results suggest that GRL leaf extract exert preventive and curative effects against STZ-induced diabetic neuropathy in rats which might be due to its antioxidant, anti-inflammatory, and antiapoptotic properties.Graphical abstractProtection against neuropathy

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Abstract. A study was conducted to investigate the capability of Myrtus communis essential oil (MCE) in counteracting the deleterious effects of aflatoxin B1 (AFB1) on growth performance, serum biochemistry and humoral immune responses in broiler chickens. In a completely randomized design, 300 day-old male chicks were assigned to four treatments with five replicates of 15 birds for 42 days. Chickens, up to day 7 of age, were fed the same diet and then, they were fed the experimental diets. The dietary treatments were 1) the negative control (no dietary aflatoxin or MCE), 2) the positive control (diet containing AFB1 at 0.5 mg/kg, without MCE), 3) diet containing AFB1 at 0.5 mg/kg plus 500 mg/kg MCE, and 4) basal diet containing 500 mg/kg MCE, without AFB1. Growth performance was measured from day 7 to 42. Serum biochemical parameters, organ weights on day 42 and the antibody titers against Newcastle and influenza viruses on day 28 of age were determined. Addition of aflatoxin to diet decreased (P<0.05) the weight gain and feed intake and MCE supplementation diminished (P<0.05) the inhibitory effects of AFB1 on the growth performance. Addition of AFB1 to diet of chicks increased the serum activities of aspartate aminotransferase (AST), alkaline aminotransferase (ALT), alkaline phosphatase (ALP), and decreased the antibody titers against Newcastle and influenza viruses. Addition of MCE to diet alleviated the negative effects of AFB1 on these parameters (P<0.05). In conclusion, our results showed that addition of MCE may reduce the adverse effects of AFB1 on broiler chickens.

It has been hypothesized that maternal hyperhomocysteinemia to be associated with preeclampsia. The aims of the present study were to examine maternal serum levels of total homocysteine in preeclamptic women and its association with the severity of the disease. The study population consisted of 30 preeclamptic patients and 30 matched healthy pregnant women. Serum levels of total homocysteine were assessed using enzyme immunoassay method. Maternal serum levels of total homocysteine were significantly higher in preeclamptic group than in normal pregnant women. Women with severe preeclampsia had higher serum levels of total homocysteine than mild preeclamptic patients. Levels of total homocysteine correlated positively with systolic blood pressure values in preeclamptic women. In summary, maternal serum levels of total homocysteine were increased in preeclamptic women and hyperhomocysteinemia was associated with severity of preeclampsia.

BackgroundRecent studies shows that hyperbaric oxygen (HBO) therapy exerts some protective effects against neural injuries. The purpose of this study was to determine the neuroprotective effects of HBO following sciatic nerve transection (SNT).MethodsRats were randomly divided into five groups (n = 14 per group): Sham-operated (SH) group, SH + HBO group, SNT group, and SNT + pre- and SNT + post-HBO groups (100% oxygen at 2.0 atm absolute, 60 min/day for five consecutive days beginning on 1 day before and immediately after nerve transaction, respectively). Spinal cord segments of the sciatic nerve and related dorsal root ganglions (DRGs) were removed 4 weeks after nerve transection for biochemical assessment of malodialdehyde (MDA) levels in spinal cord, biochemical assessment of superoxide dismutase (SOD) and catalse (CAT) activities in spinal cord, immunohistochemistry of caspase-3, cyclooxigenase-2 (COX-2), S100beta (S100ß), and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) in spinal cord and DRG.ResultsThe results revealed that MDA levels were significantly decreased in the SNT + pre-HBO group, while SOD and CAT activities were significantly increased in SNT + pre- and SNT + post-HBO treated rats. Attenuated caspase-3 and COX-2 expression, and TUNEL reaction could be significantly detected in the HBO-treated rats after nerve transection. Also, HBO significantly increased S100ß expression.ConclusionsBased on these results, we can conclude that pre- and post-HBO therapy had neuroprotective effects against sciatic nerve transection-induced degeneration.

Background: Oleuropein is a potent antioxidant and free-radical scavenger with antiinflammatory properties. Objectives: In the present study, we evaluated the protective effects of oleuropein on myeloperoxidase (MPO) activity, nitrite, urea, creatinine and glomerulosclerosis in alloxan-induced type 1 diabetic rats. Materials and Methods: Thirty Sprague-Dawley male rats were randomly divided into 3 groups: group 1 as control; group 2 as untreated diabetic; and group 3 as treated with oleuropein 15 mg/kg i.p daily. Diabetes was induced in the second and third groups by subcutaneous alloxan injection. After 48 days, the animals were anaesthetized and then the livers and kidneys were removed immediately and used fresh or kept frozen until MPO activity analysis. Blood samples were also collected before sacrificing to measure nitrite, urea, and creatinine. Kidney paraffin sections were prepared to estimate glomerular volume, leukocyte infiltration, and glomerulosclerosis. Results: Oleuropein significantly decreased leukocyte infiltration and glomerulosclerosis in the treated group compared with the diabetic untreated group. Oleuropein significantly decreased the levels of urea, nitrite, and creatinine in the treated group compared with the diabetic untreated group. Moreover, oleuropein significantly decreased MPO activity in the treated group compared with the diabetic untreated group. Conclusions: Oleuropein has antioxidative and antiatherogenic activities and exerts beneficial effects on inflammation and kidney function test and decreases diabetic complication in diabetic rats.

Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR significantly decreased the serum and renal levels of GSH, serum paraoxonase 1 (PON1) activity, and the serum and renal activities of catalase (CAT) and glutathione peroxidase (GPX). GSH administration could significantly improve the serum activities of AST, GGT, MPO, GPX and PON1 and serum levels of NO, renal MDA, GSH levels, and serum and also renal CAT activities. Conclusion: Our study indicated that GSH administration ameliorated RIR injury in rats by improving the activities of liver markers and antioxidant enzymes, the levels of MDA, NO, GSH and MPO activity.

Introduction: Selenium (Se) is an antioxidant and reactive oxygen species (ROS) scavenger. Objectives: This study was conducted to evaluate the effects of Se on renal functional parameters, oxidative stress biomarkers, myeloperoxidase (MPO) activity, and the nitric oxide (NO) level in renal ischemia-reperfusion (IR) injury in rats. Materials and Methods: Twenty-four male Wistar rats (180–200 g) were selected and subsequently divided into three groups (n=8); group 1 as the control group, group 2 as the untreated group (IR without treatment) and group 3 as the IR group (treated with Se (1 mg/kg/d, intraperitoneally). The period of Se administration was 2 weeks before the inducing renal IR. To cause renal IR, renal pedicles were occluded by safe clamps for 45 minutes. Then, the clamps were removed and 24 hours was considered as reperfusion. After the study, blood sampling from the hearts and the removal of the left kidney was conducted immediately for biochemical measurements. Results: Renal IR significantly increased serum levels of urea, creatinine (Cr), serum and renal malondialdehyde (MDA) levels, serum NO level, and MPO activity. It significantly decreased serum and renal glutathione (GSH) levels, serum paraoxonase 1 activity, serum and renal activities of catalase (CAT), and glutathione peroxidase (GPx). Se could reverse these findings, but the increase of paraoxonase 1 activity and the decrease of MPO activity in IR animals were not significant. Conclusion: It seems that Se has protective effects on inflammatory indices. It can ameliorate renal IR complications which are associated with oxidative stress and inflammation.