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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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.

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.

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