Electroacupuncture (EA) has demonstrated therapeutic potential for the treatment of Alzheimer's disease (AD). A previous study reported that N-myc downstream-regulated gene 2 (NDRG2) was upregulated in the brain of patients with AD. In the present study, we investigated the effects of repeated EA administration on reference memory impairment and the role of NDRG2 in an amyloid precursor protein (APP)/presenilin-1 (PS1) double transgenic mouse model. Age-matched wild-type and transgenic mice were treated with EA (once per day for 30 min) for 4 weeks (four courses of 5 days EA administration and 2 days rest) beginning at 10 months of age. At seven and ten postnatal months of age and following a 4-week EA treatment regime, mice received training in the Morris water maze (MWM) and a probe test. Brain tissue was analyzed via Western blot and double-label immunofluorescence. Beginning at 7 months of age, APP/PS1 mice began to exhibit deficits in reference memory in the MWM test, an impairment associated with upregulation of glial fibrillary acidic protein (GFAP) and NDRG2. Four weeks of EA administration significantly ameliorated cognitive impairments and suppressed GFAP and NDRG2 upregulation. In conclusion, our findings demonstrated that EA administration can alleviate reference memory deficits and suppress NDRG2 upregulation in an AD transgenic mouse model. This study provides supportive evidence for EA as an effective therapeutic intervention for AD, as well as NDRG2 as a novel target for AD treatment.
Objectives: To evaluate the effects of different doses of ascorbic acid (AA) on the functional performance of rats subjected to standardized spinal cord injury (SCI). Methods: Thirty female Sprague-Dawley rats were divided into three groups (10 animals in each group): control group: rats were subjected to SCI injury and received intraperitoneal saline administration; normal-dose AA group: rats were subjected to SCI injury and received daily intraperitoneal administration of AA at 100 mg kg À1 bodyweight; high-dose AA group: rats were subjected to SCI injury and received daily intraperitoneal administration of AA at 200 mg kg À1 bodyweight. The Basso, Beattie, Bresnahan Locomotor Rating Score (BBB score) and footprint analysis were performed to evaluate the functional performance of the rats in each group, and hematoxylin and eosin staining was performed to evaluate necrosis at the injury site. Results: At days 14 and 28 after SCI, rats in the high-dose AA group, but not the normal-dose AA group, exhibited significantly better BBB score compared with the control group (Po0.05). Compared with the control and normal-dose AA group, the high-dose AA group also showed increased stride length, decreased stride width and reduced toe dragging (Po0.05). Histological analysis revealed that both the normal-and high-dose AA groups had reduced necrosis in the injury site compared with the control group (Po0.05). Conclusion: High-dose AA administration during the acute phase post SCI significantly reduced secondary injury-induced tissue necrosis and improved functional performance in rats.
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