ABSTRACT
Objective To explore the effects of electroacupuncture on brain derived neurotrophic factor (BDNF) of rats with sciatic nerve injury (SNI); To discuss its biological mechanism for treatment of SNI. Methods Fifty adult male Wistar rats were chosen, and the sciatic nerves of rats were cut off and pulled on both sides of the cut ends into nerve regeneration chamber. The rats were randomly divided into normal group, sham-operation group, model group, and electroacupuncture group. In the electroacupuncture group, the rats were treated by electroacupuncture for 28 days. After the treatment, the nerve regeneration was observed through HE staining. Immunofluorescence was used to analyze the expression changes of BDNF in the nerve tissue and spinal cord. ELISA was used to observe the changes of expression of serum BDNF. Results The amount of axon regeneration in the electroacupuncture group was obviously more than that in the model group, and the outline of the tissue more clear. Electroacupuncture could promote the expression of BDNF in the nerve, spinal cord and serum of SNI of rats compared with model group (P<0.01). Conclusion Electroacupuncture can promote the repairment and regeneration of SNI in rats by upregulating the expression of BDNF.
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Objective To observe the effects of electroacupuncture on the expressions of autophagy related protein Beclin-1 and apoptosis related protein p53 of hippocampus in rats;To explore the mechanism of electroacupuncture on Alzheimer's disease (AD).Methods The rats were randomly divided into the normal group, the sham-operation group, the model group, and the electroacupuncture treatment group. “Baihui” and “Yongquan” points were taken for electroacupuncture treatment and the treatment course was 7 days. The rats were treated once a day for 4 courses. Changes in morphology and number of Nissl positive cells were examined by Nissl staining in hippocampal CA1 regions. Expressions of Beclin-1 and p53 protein were determined by Western blot analysis.Results Number of Nissl positive cells in CA1 region of the model group was significantly less than that of normal group (P<0.01). After electroacupuncture treatment, number of pyramidal cells and expression of Nissl body significantly increased (P<0.05). Expression of Beclin-1 decreased, while expression of p53 increased in the hippocampus of the model group, compared with that in the normal group (P<0.05). However, electroacupuncture treatment could significantly upregulate the expression of Beclin-1 protein (P<0.01), but downregulate the level of p53 (P<0.05).Conclusion Electro-acupuncture treatment could fight against Aβ-induced neuronal apoptosis, and improve the morphological changes of AD’s hippocampus.
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Objective To explore the protective effects of electro-acupuncture (EA) serum onβ-amyloid protein (Aβ) induced primary rat hippcampal neurons. Methods The rat models of Alzheimer's disease were established by intracerebral injection of Aβ1-40. After treated them with EA, the serum was harvested. Primary cultured hippocampal neurons were treated with Aβ25-35 to establish neuronal damage model in vitro, and divided into normal group, model group and EA serum group. The proliferation of neurons was detected by MTT test. Neuronal apoptosis was examined by TUNEL staining, and expression of cysteine aspartic acid proteases-3 (Caspase-3) was detected by immunocytochemical staining. Results MTT test showed that the cell viability was significantly decreased after treated with Aβ. While compared with the model group, cell proliferation of EA serum group was significantly enhanced (P<0.01). TUNEL staining showed that the number of apoptotic cells in EA serum group decreased significantly compared with the model group (P<0.01). After 48 h of Aβ treatment, Caspase-3 expression levels were significantly elevated. However, compared with the model group, the number of Caspase-3 positive cells in EA serum group was significantly reduced (P<0.01). Conclusion The EA serum could promote the proliferation of hippocampal neurons, reduce the expression of Caspase-3, counteract the neurotoxicity of β-amyloid protein, and reduce neuronal apoptosis.