Effects of recombinant human erythropoietin on brain-derived neurotrophic factor expression in different brain regions of aging rats / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the effect of recombinant human erythropoietin (rhEPO) on expression of brain-derived neurotrophic factor (BDNF) in different brain regions of aging rats.</p><p><b>METHODS</b>Forty male SD rats were randomized equally into negative control group, D-galactose group, EPO treatment group, and positive control group. Rat models of subacute aging were established by continuous subcutaneous injection of 5% D-galactose. Immunohistochemical staining was used to analyze the variation of BDNF expressions in different brain regions of the aging rats with different treatments.</p><p><b>RESULTS</b>Significant brain region-specific differences in BDNF expression were found among the rats in different groups. Compared with those in the negative control group, the numbers of BDNF-positive cells in the hippocampal CA1 region, CA3 region, dentate gyrus (DG) and frontal cortex were all decreased obviously in D-galactose group (P<0.05) but increased in both EPO group and the positive control group (P<0.05) without significant differences between the latter two groups. In the rats in the same group, the number of BDNF-positive cells varied markedly in different brain regions (P<0.05), and the expression level of BDNF was the highest in the frontal cortex followed by the hippocampal CA3 region and the dentate gyrus, and was the lowest in the hippocampal CA1 region.</p><p><b>CONCLUSION</b>Treatment with rhEPO enhances the expression of BDNF in rat neural cells, suggesting that rhEPO may protect the nervous system from aging by regulating the BDNF pathway.</p>

Continuous epidural block of the cervical vertebrae for cervicogenic headache / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Cervicogenic headache (CEH) is caused by a structural abnormality in the cervical spine. Available treatments for CEH include medical therapy, local botulinum toxin injection, cervical epidural corticosteroid injection, and surgery. The objective of this study was to investigate the safety and efficacy of a continuous epidural block of the cervical vertebra.</p><p><b>METHODS</b>Medical records were retrospectively analyzed for 37 patients diagnosed with CEH treated by a continuous epidural block of the cervical vertebra with lidocaine, dexamethasone, and saline (5 ml/min) for 3 - 4 weeks and triamcinolone acetonide 5 mg once weekly for 3 - 4 weeks. Pain was measured via the visual analogue scale (VAS) in combination with quality of life assessment. Outcome measures were patient-reported days with mild or moderate pain, occurrence of severe pain, and the daily oral dosages of non-steroidal anti-inflammatory drug use (NSAID).</p><p><b>RESULTS</b>In the 3 months immediately preceding placement of the epidural catheter, the mean number of days with mild or moderate pain was 22.0 +/- 4.3. The mean occurrence of severe pain was (3.20 +/- 0.75) times and the mean oral dosage of NSAID was (1267 +/- 325) mg. During the first 6 months after epidural administration of lidocaine and corticosteroids, the mean number of days with mild or moderate pain, the mean occurrence of severe pain, and the mean daily oral dosages of NSAIDs were significantly decreased compared to 3-month period immediately preceding treatment (P < 0.01). By 12 months post-treatment, no significant difference in these three outcome measures was noted.</p><p><b>CONCLUSIONS</b>Continuous epidural block of the cervical vertebra for patients with CEH is effective for at least six months. Further research is needed to elucidate mechanisms of action and to prolong this effect.</p>

Expression of Ref-1 in hippocampus CA1 area of rats with Alzheimer's disease / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To investigate the expression of Redox factor-1(Ref-1) in rats with Alzheimer's disease (AD).</p><p><b>METHODS</b>AD rat model was established by a single injection of beta-amyloid peptide (Abeta25-35) into the lateral cerebral ventricle of rats. Y-shape maze task was conducted to check the ethology. At 4th, 7th and 14th day after injection, Ref-1 expression in hippocampus CA1 area was detected by immunohistochemistry.</p><p><b>RESULT</b>The numbers of repeated learning and error and the total reaction time in AD group were significantly higher than those in control group at 7th and 14th day after injection of Abeta25-35 (P<0.05). At 4th day after injection of Abeta25-35, the Ref-1 expression was increased with time prolongation in AD group(P<0.01).</p><p><b>CONCLUSION</b>Injection of Abeta25-35 in lateral cerebral ventricle can decrease the learning and memory abilities of rats, and results also indicate that Ref-1 expression in hippocampus may be involved in the development of AD.</p>

Expression of p38MAPK in the hippocampal CA1 region of rats with Abeta25-35-induced Alzheimer disease / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the changes of p38MAPK expression in a rat model of Alzheimer disease (AD).</p><p><b>METHODS</b>Seventy-two adult SD rats were randomized equally into 4 groups, and a single-dose injection of Abeta25-35 (dementia group), normal saline (saline group), SB203580 (inhibitor group), or DMSO (inhibitor control group) was administered into the lateral cerebral ventricle. Y-maze tast was performed to evaluate the behavioral changes of the rats after the injections, and on days 4, 7 and 14 after the injection, p38MAPK expression in the hippocampal CA1 area was measured by means of immunohistochemistry.</p><p><b>RESULTS</b>On days 7 and 14 following Abeta25-35 injection, the training times, error number and total reaction time were significantly higher in dementia group than in saline group (P<0.05), but all these indices were significantly lowered in the inhibitor group as compared with the dementia group (P<0.05). Immunohistochemistry revealed obvious p38 expression in the dementia group 4 days after Abeta25-35 injection, which increased significantly with the passage of time (P<0.01). The gray scale in the inhibitor group was significantly higher than that in the dementia group (P<0.01).</p><p><b>CONCLUSION</b>p38MAPK activation in the hippocampal CA1 area is an event that persists during the entire course of Abeta25-35-induced AD in rats, and the inhibitor SB203580 prevents p38MAPK expression and improves the learning and memory abilities of the rats.</p>