Comparison of the therapeutic effects of erythropoietin and acetyl-l-carnitine on sciatic nerve injury in rats.

AIM: We aimed to investigate the effects of erythropoietin, acetyl-l-carnitine, and their combination on nerve regeneration in experimental peripheral nerve injury. METHODS: Rats were randomly divided into five groups - sham-operated (S), sciatic nerve crush injury (C), C + acetyl-l-carnitine (ALCAR), C + erythropoietin (EPO), and C + EPO + ALCAR. ALCAR (50 mg/kg/day) was administered intraperitoneally, and EPO (5000 U/kg) was injected subcutaneously for 10 days. Functional recovery was evaluated using walking track analysis (sciatic functional index [SFI]), somatosensory evoked potentials (SEPs), thiobarbituric acid reactive substance (TBARS) assay, and caspase-3 and S100 immunoreactivities. RESULTS: In SFI analyses, delayed functional recovery was observed in the C group, whereas the functional recovery of rats treated with EPO and ALCAR significantly improved. The latencies of the SEP components were significantly prolonged in C group. In the treatment groups (C + EPO, C + ALCAR, and C + EPO + ALCAR), all recorded values of SEP components significantly decreased. TBARS levels in C group were significantly higher than those in the S group. EPO and ALCAR administration significantly decreased TBARS levels. Caspase-3 immunoreactivity was increased in the C group, whereas it was decreased in the treatment groups. S100 immunolabelling was significantly decreased in the C group. EPO and ALCAR administration caused an increase in the amount of S100-positive cells in all treatment groups. CONCLUSION: EPO and ALCAR administration could accelerate sciatic nerve repair by reducing apoptosis and lipid peroxidation and promoting myelinization. Although both EPO and ALCAR had positive effects on nerve healing, their combined efficacy had no statistically significant effect on peripheral nerve regeneration.

The effects of sulfite on cPLA2, caspase-3, oxidative stress and locomotor activity in rats.

Sulfite is a commonly used preservative in food products, alcoholic beverages and pharmaceutical products. We investigated the effect of sulfite, on locomotor activity as well as the relationship of these effects with oxidant and antioxidant capacities, cPLA2 enzyme activity. Thirty male Wistar albino rats were randomly divided into two groups as control(C) and sulfite(S). Animals in the S group were given freshly prepared sulfite for 35 days via gastric gavage (100 mg/kg/day) while the C group received equal volumes of distilled water via gavage for the same period. Open-field tests were performed to all groups and animals were sacrificed. Total antioxidant capacity(TAC), TBARS levels, cPLA2 activity as well as amount of caspase-3 positive cells were analyzed on the hippocampi. In the open field test, distance and velocity values of the S group increased with respect to controls. TBARS and cPLA2 activity were also increased in the S group, while levels of TAC decreased compared to controls. Immunohistochemical analysis showed that sulfite ingestion caused an increase in the amount of hippocampal caspase-3 positive cells. In conclusion, sulfite seemed to increase locomotor activity. cPLA2 might play a role in ingested sulfite-induced oxidative stress and apoptotic cell death in the hippocampus.

The antidepressant-like activity of ellagic acid and its effect on hippocampal brain derived neurotrophic factor levels in mouse depression models.

The aim of present study was to evaluate the antidepressant-like activity of ellagic acid (EA) in mice-forced swim test (FST) and tail suspension test (TST) and the possible role of brain-derived neurotrophic factor (BDNF) in EA's antidepressant-like effect. We found that EA and sertraline did not affect the spontaneous locomotor activity of mice. EA produced statistically significant decrease in immobility time as compared to vehicle group in TST. EA at 1 and 5 mg/kg doses did not produce any significant effect in immobility time as compared to vehicle group in FST. But EA produced significantly reduced immobility time at 2.5 mg/kg dose. EA treatment increased hippocampal BDNF level. This study demonstrates that EA is able to produce antidepressant-like effect in both TST and FST in mice. Moreover, the antidepressant-like effects of EA seems to be mediated by increased BDNF level in mice hippocampus.

Effects of acute and chronic exposure to both 900 MHz and 2100 MHz electromagnetic radiation on glutamate receptor signaling pathway.

PURPOSE: To demonstrate the molecular effects of acute and chronic exposure to both 900 and 2100 MHz radiofrequency electromagnetic radiation (RF-EMR) on the hippocampal level/activity of some of the enzymes - including PKA, CaMKIIα, CREB, and p44/42 MAPK - from N-methyl-D-aspartate receptor (NMDAR)-related signaling pathways. MATERIALS AND METHODS: Rats were divided into the following groups: sham rats, and rats exposed to 900 and 2100 MHz RF-EMR for 2 h/day for acute (1 week) or chronic (10 weeks), respectively. Western blotting and activity measurement assays were used to assess the level/activity of the selected enzymes. RESULTS: The obtained results revealed that the hippocampal level/activity of selected enzymes was significantly higher in the chronic groups as compared to the acute groups at both 900 and 2100 MHz RF-EMR exposure. In addition, hippocampal level/activity of selected enzymes was significantly higher at 2100 MHz RF-EMR than 900 MHz RF-EMR in both acute and chronic groups. CONCLUSIONS: The present study provides experimental evidence that both exposure duration (1 week versus 10 weeks) and different carrier frequencies (900 vs. 2100 MHz) had different effects on the protein expression of hippocampus in Wistar rats, which might encourage further research on protection against RF-EMR exposure.

Effect of sodium tungstate on visual evoked potentials in diabetic rats.

AIM: To evaluate the effect of sodium tungstate on visual evoked potentials (VEPs) in diabetic rats. METHODS: Wistar rats were randomly divided into three groups as normal control, diabetic control and diabetic rats treated with sodium tungstate. Diabetes was induced by single intraperitoneal injection of streptozotocin (50 mg/kg). Sodium tungstate [40 mg/(kg·d)] was administered for 12wk and then VEPs were recorded. Additionally, thiobarbituric acid reactive substance (TBARS) levels were measured in brain tissues. RESULTS: The latencies of P1, N1, P2, N2 and P3 waves were significantly prolonged in diabetic rats compared with control group. Diabetes mellitus caused an increase in the lipid peroxidation process that was accompanied by changes in VEPs. However, prolonged latencies of VEPs for all components returned to control levels in sodium tungstate-treated group. The treatment of sodium tungstate significantly decreased brain TBARS levels and depleted the prolonged latencies of VEP components compared with diabetic control group. CONCLUSION: Sodium tungstate shows protective effects on visual pathway in diabetic rats, and it can be worthy of further study for potential use.