Astragalus Polysaccharide Promotes Neuronal Injury Repair via the Notch1/NFκB Signaling Axis in the Ventroposterior Thalamic Nucleus in Rats with Focal Cerebral Ischemia.

BACKGROUND: Ischemic stroke is the most common form of stroke and the second most common cause of death and incapacity worldwide. Its pathogenesis and treatment have been the focus of considerable research. In traditional Chinese medicine, the root of Mongolian astragalus has been important in the treatment of stroke since ancient times. Astragalus polysaccharide (APS) is a key active ingredient of astragalus and offers therapeutic potential for conditions affecting the neurological system, the heart, cancer, and other disorders. However, it is not yet known how APS works to protect against ischemic stroke. METHODS: Rats were subjected to middle cerebral artery occlusion (MCAO) to imitate localized cerebral ischemia. Each of four experimental groups (normal, sham, MCAO, and MCAO+APS) contained 12 adult male Sprague-Dawley (SD) rats selected randomly from a total of 48 rats. Following successful establishment of the model, rats in the MCAO+APS group received intraperitoneal injection of APS (50 mg/kg) once daily for 14 days, whereas all other groups received no APS. The Bederson nerve function score and the forelimb placement test were used to detect motor and sensory function defects, while Nissl staining was used to investigate pathological defects in the ventroposterior thalamic nucleus (VPN). Immunohistochemical staining and Western blot were used to evaluate the expression of Neurogenic locus notch homolog protein 1 (Notch1), hairy and enhancer of split 1 (Hes1), phospho-nuclear factor-κB p65 (p-NFκB p65), and nuclear factor-κB p65 (NFκB p65) proteins in the VPN on the ischemic side of MCAO rats. RESULTS: APS promoted the recovery of sensory and motor function, enhanced neuronal morphology, increased the number of neurons, and inhibited the expression of Notch1/NFκB signaling pathway proteins in the VPN of rats with cerebral ischemia. CONCLUSION: After cerebral ischemia, APS can alleviate symptoms of secondary damage to the VPN, which may be attributed to the suppression of the Notch1/NFκB pathway.

Electroacupuncture protects against the striatum of ischemia stroke by inhibiting the HMGB1/RAGE/p-JNK signaling pathways.

The striatum (Str) is injured 20 min after permanent ischemic stroke, leading to neurological deficits. Here, we aimed to explore the effect of electroacupuncture (EA) on ischemic stroke and elucidate the possible underlying mechanism. Rat permanent middle cerebral artery occlusion (pMCAO) model, EA treatment, sham-EA (SEA) treatment, beam-balance test, hematoxylin and eosin (HE) staining, Nissl staining, immunofluorescence staining, and Western blot were used to investigate the role of EA in pMCAO. The results showed that balance ability and motor coordination were obviously injured after pMCAO. EA improved balance ability and motor coordination in pMCAO rats. EA reduced striatal injury by reducing the expression of high-mobility group box 1(HMGB1)/receptor for advanced glycation end products (RAGE)/phosphorylated C-Jun N-terminal kinase (p-JNK), whereas SEA did not. Thus, EA plays a neuroprotective role during pMCAO injury, which may be related to the inhibition of HMGB1/RAGE/p-JNK expression.

Electroacupuncture reduces cerebral ischemia-induced neuronal damage in the hippocampal CA1 region in rats by inhibiting HMGB1 and p-JNK overexpression.

BACKGROUND: The cornu ammonis 1 (CA1) region of the hippocampus is a sensitive area that is susceptible to injury caused by cerebral ischemia. High-mobility group box 1 (HMGB1) and phosphorylated c-Jun N-terminal kinase (p-JNK) play important roles in mediating cerebral ischemic injury. OBJECTIVE: To elucidate the mechanism through which electroacupuncture (EA) via the Baihui (GV20) and Zusanli (ST36) acupoints protects neurons. METHODS: A rat model of permanent middle cerebral artery occlusion (pMCAO) was established. Sprague-Dawley rats were divided into four groups: sham-operated control, pMCAO control, EA, and sham-EA (SEA). In the EA and SEA groups, the GV20 and ST36 acupoints were selected for treatment. However, the SEA group was treated only by superficial pricking of the skin at the two acupoints without the application of electricity. Neurological function was assessed using the neurological deficit function score, and neuronal damage was detected through Nissl staining. HMGB1 and p-JNK expression was evaluated using immunohistochemical staining and western blot assays. RESULTS: The behavioural experiments showed that the EA treatment improved the neurological deficits in the pMCAO rats. The Nissl staining results revealed that EA reduced neural tissue damage. The immunohistochemical staining and western blot results showed that EA inhibited HMGB1 and p-JNK overexpression. By contrast, none of these EA effects were observed in the SEA group. CONCLUSION: EA may reduce ischemia-induced neuronal damage in the hippocampal CA1 region by inhibiting the overexpression of both HMGB1 and p-JNK.

Electroacupuncture inhibits the expression of HMGB1/RAGE and alleviates injury to the primary motor cortex in rats with cerebral ischemia.

Background: The high-mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) signaling pathway holds promise as a potential therapeutic target for ischemic brain injury. The effects of FPS-ZM1 and electroacupuncture (EA) on activation of the HMGB1/RAGE signaling pathway after cerebral ischemia remain uncertain. Methods: Middle cerebral artery occlusion (MCAO) model was established. Neurological function was assessed using Longa scores. Nissl staining was used to observe the morphology of neurons. The expression levels of HMGB1 and RAGE were assayed with immunofluorescence staining and western blot. Results: The results showed that EA and FPS-ZM1 could reduce the neural function score and neurons cell injury in cerebral ischemia rats by inhibiting the expression of HMGB1 and RAGE in primary motor cortex (M1) region. In addition, EA combined with FPS-ZM1 had a better therapeutic effect. Conclusions: The HMGB1/RAGE pathway could be activated after cerebral ischemia. Both EA and FPS-ZM1 improved neurological deficits and attenuated neuronal damage in rats. They had synergistic effects. These interventions were observed to mitigate brain damage by suppressing the activation of HMGB1/RAGE.

Electroacupuncture attenuates ketamine-induced neuronal injury in the locus coeruleus of rats through modulation of the CAMK II/CREB pathway.

BACKGROUND: Ketamine, despite its efficacy in treating depression, raises concerns regarding safety due to potential abuse, cognitive impairment, and bladder toxicity. Ketamine can affect the locus coeruleus (LC) norepinephrine and attention networks. This study explored the protective effects of electroacupuncture (EA) on the LC of rats exposed to repeated administration of ketamine while investigating the potential role of the Calcium CaM-dependent protein kinase II (CAMK II)/ cAMP response element binding protein (CREB) pathway in mediating EA's impact on ketamine-induced neuronal injury in LC. METHODS: Rats were repeatedly injected intraperitoneally with ketamine hydrochloride (50 mg/kg) once daily for seven days. Subsequently, EA was performed at the acupoints "Zusanli" (ST36) and "Sanyinjiao" (SP-6) once daily following ketamine administration. The Morris water maze test was employed to assess behavioral changes in the rats. Neuronal injury was examined using Nissl staining, and the expression of CAMK II, CREB, and phospho-CREB (p-CREB) was evaluated through immunohistochemistry and western blotting. RESULTS: EA mitigated the cognitive and exploratory impairments and attenuated neuronal injury in the LC induced by repeated administration of ketamine. The expression of CAMK II and p-CREB proteins in the LC increased following 7 days of ketamine administration. However, EA treatment led to a downregulation of CAMK II and p-CREB expression. CONCLUSION: Repeated administration of ketamine in male rats can lead to neuronal injury and neurobehavioral dysfunction. However, EA was found to ameliorate neurodegeneration in the LC and enhance neurobehavioral symptoms. This therapeutic effect of EA may be attributed to its modulation of the CAMKII/CREB pathway, thereby mitigating the aforementioned adverse effects.

Regulatory Effect of Electroacupuncture on Hypothalamic Serotonin and its Receptor in Rats with Cerebral Ischemia.

BACKGROUND: Previous studies have shown that the neurological damage caused by middle cerebral artery occlusion (MCAO) is not only limited to local infarction but can also cause secondary damage in distant sites, such as the hypothalamus. 5-hydroxytryptamine (5-HT)/ 5-HT transporter (5-HTT) and 5-HT receptor 2A (5-HT2A) are important in the treatment of cerebrovascular diseases. OBJECTIVE: This study aimed to study the effect of electroacupuncture (EA) on the expression of 5- HT, 5-HTT, and 5-HT2A in the hypothalamus of rats with ischemic brain injury and to explore the protective effect and potential mechanism of EA on the secondary injury of cerebral ischemia. METHODS: Sprague-Dawley (SD) rats were randomly divided into three groups: sham group, model group, and EA group. The permanent middle cerebral artery occlusion (pMCAO) method was used to induce ischemic stroke in rats. In the EA group, the Baihui (GV20) and Zusanli (ST36) points were selected for treatment, which was administered once per day for two consecutive weeks. The neuroprotective effect of EA was evaluated by nerve defect function scores and Nissl staining. The content of 5-HT in hypothalamus was detected by enzyme linked immunosorbent assay (ELISA), and the expression of 5-HTT and 5-HT2A were detected by Western blot. RESULTS: Compared with that in the sham group, the nerve defect function score in the model group rats was significantly increased, the hypothalamus tissue showed obvious nerve damage, the levels of 5-HT and the expression of 5-HTT were significantly reduced, and the expression of 5-HT2A was significantly increased. After 2 weeks of EA treatment, the nerve defect function scores of pMCAO rats were significantly reduced, the hypothalamic nerve injury was significantly reduced, the levels of 5-HT and the expression of 5-HTT were significantly increased, and the expression of 5-HT2A was significantly decreased. CONCLUSION: EA has a certain therapeutic effect on hypothalamic injury secondary to permanent cerebral ischemia, and its potential mechanism may be closely related to the upregulation of 5-HT and 5-HTT expression and the downregulation of 5-HT2A expression.

Electroacupuncture Inhibits Myelin Sheath Injury in the Internal Capsule After Focal Cerebral Infarction in Rats Through the Nogo-A/NgR Signaling Pathway.

BACKGROUND Ischemic stroke is usually accompanied by white matter damage. The effect of electroacupuncture (EA) on ameliorating white matter damage is still unclear. The purpose of this study was to explore the precise mechanism of EA in treating ischemic white matter. MATERIAL AND METHODS In this study, 40 Sprague-Dawley rats were randomly divided into 4 groups: normal group, the sham-operated group, model group, and EA group. The stroke model was established by right middle cerebral artery occlusion, and EA was performed 24 h after the operation for 30 min per day. After 14 days of treatment, brain tissue samples were collected. Hematoxylin and eosin and Luxol fast blue staining were used to observe the changes of white matter damage in the internal capsule (IC). The expression levels of myelin basic protein (MBP), Nogo-A, and Nogo-A receptor (NgR) were detected by immunohistochemistry and western blot. RESULTS Compared with the sham-operated group, the model group had decreased expression of MBP and significantly increased expression of Nogo-A and NgR (P<0.05). Compared with the model group, the IC damage was alleviated in the EA group. Immunohistochemistry and western blot analysis showed that EA significantly increased the expression of MBP in white matter (P<0.05) and downregulated the expression levels of Nogo-A and NgR (P<0.05). CONCLUSIONS The results of this study indicate that EA can inhibit the expression of Nogo-A/NgR and promote myelin sheath regeneration.

[Effects of electroacupuncture on myelin-related protein in corpus callosum of rats with focal cerebral ischemia].

OBJECTIVE: To observe the effect of electroacupuncture(EA)on the expression of myelin basic protein (MBP), axon growth inhibitor Nogo-A and Nogo receptor (NgR) in corpus callosum of rats with focal cerebral ischemia, so as to explore the mechanism of EA underlying improving ischemic white matter injury. METHODS: Fourty male SD rats were randomly divided into normal, sham operation, model and EA groups, with 10 rats in each group. The focal cerebral ischemia rat model was established by occlusion of the middle cerebral artery (MCAO). EA was applied to "Baihui"(GV20) and "Zusanli"(ST36) on the left side for 30 min, once daily for 14 days. Neurological function score and the adhensive removal test were used to evaluate neurological deficit severity; Hematoxylin-esion staining was used to observe the pathological changes in myelin of corpus callosum and luxol fast blue（LFB） staining was used to observe the myelin of corpus callosum. Immunohistochemical staining and Western blot were used to detect the expressions of MBP、Nogo-A and NgR in the ischemic corpus callosum. RESULTS: After MCAO, the neurological function score was significantly increased (P<0.05), the time required for contact with tape and tape removal was longer (P<0.001), the intensity of LFB staining and the expression of MBP decreased, while the veside area and the expression of Nogo-A and its receptor NgR increased (P<0.01, P<0.05) in the model group relevant to the normal and sham operation groups. The fiber arrangement of the corpus callosum on the ischemic side was disordered and a large amount of myelin sheath was lost in the model group. Following the treatment, the neurological deficit score of EA group was gradually decreased and significantly decreased on the 3rd, 7th and 14th day (P<0.05), and the time to remove the adhesive tape was shortened at the 7th and 14th day (P<0.001). The shape of the corpus callosum in the EA group was close to normal, and the myelin structure was relatively complete. The intensity of LFB staining and the expression of MBP was increased (P<0.05, P<0.01) while the expression of Nogo-A and its receptor NgR were decreased in the EA group relevant to the model group (P<0.01). CONCLUSION: EA can play a protective role in myelin of the corpus callosum after cerebral ischemia, which may be related to down-regulating the expressions of Nogo-A and NgR.

Effects of Electroacupuncture on Expression of D1 Receptor (D1R), Phosphorylation of Extracellular-Regulated Protein Kinase 1/2 (p-ERK1/2), and c-Fos in the Insular Cortex of Ketamine-Addicted Rats.

BACKGROUND The aim of this study was to investigate the effects of electroacupuncture (EA) on expression of the D1 receptor (D1R), phosphorylation of extracellular-regulated protein kinase 1/2 (p-ERK1/2) and c-Fos in the insular cortex (IC) of ketamine-addicted rats. MATERIAL AND METHODS Sprague-Dawley rats were randomly divided into 7 groups: the normal group, the normal saline (NS) group, the ketamine (Ket) group, the U0126+Ket group, the SCH23390+Ket group, the Ket+acupoints EA (EA1) group, and the Ket+ non-acupoints EA (EA2) group. We used immunohistochemistry to detect the expression of D1R, p-ERK1/2, and c-Fos. We also used Nissl staining techniques to study the morphology of IC neurons. RESULTS Our study demonstrated that the ketamine group had sparsely distributed neurons, large intracellular vacuoles, nuclei shift, and unclear nucleolus. The number of Nissl-positive (neuronal) cells in the ketamine group were decreased than in the normal group. Our results also indicated that there was significantly lower expression of D1R, p-ERK1/2, and c-Fos in the IC of the U0126+Ket group, SCH23390+Ket group, and Ket+EA1 group as compared with that of the Ket group. CONCLUSIONS Ketamine addiction induces c-Fos overexpression in the IC by increasing the expression of D1R and p-ERK1/2. Acupoints EA downregulate D1R and p-ERK1/2 by reducing the overexpression of c-Fos.

[Effect of Electroacupuncture Intervention on Expressions of Nerve Growth Factor and Growth Arrest-specific Protein 7 in Ventral Posterolateral Thalamic Nucleus in Cerebral Ischemia Rats].

OBJECTIVE: To observe the effect of electroacupuncture(EA) on expressions of nerve growth factor(NGF) and growth arrest-specific protein 7(Gas 7) in the right ventral posterolateral nucleus(VPL) in the focal cerebral ischemia (FCI) rats, so as to explore its possible mechanism underlying improvement of secondary injury of FCI. METHODS: Forty-eight Sprague-Dawley rats were randomly divided into normal group, sham operation group, model group and electroacupuncture (EA) group (n=12 in each group) by random number table.The FCI model was made by occlusion of the right middle cerebral artery (MCAO) with thread embolus.One week after MCAO, EA(2 Hz,2 V) was performed on "Baihui"(GV 20) and left "Zusanli"(ST 36) for 30 min,once daily for successively 21 days.The expressions of NGF and Gas 7 in the right VPL were detected by immunohistochemistry (n=6 in each group) and Western blot (n=6 in each group), respectively;meanwhile Nissl staining was conducted to show VPL neurons. RESULTS: Nissl staining showed that the structure of right VPL was clear and complete,and the nuclei were centered and clear in the normal group and sham operation group;the VPL neurons were deeply stained, and the nuclei were pyknotic in the model group;the morphology of neurons in the EA group was similar to that of the normal group. The results of immunohistochemistry and Western blot were consistent. Expressions of NGF and Gas 7 proteins in the right VPL were not of significant differences between the sham operation group and the normal group (P>0.05). Compared with the normal group, the expressions of NGF and Gas 7 proteins in the VPL of the ischemic side were significantly increased in the model group(P<0.05). After treatment,the expression levels of NGF and Gas 7 proteins were further up-regulated in the EA group in comparison with the model group(P<0.05). CONCLUSIONS: The enhanced expressions of NGF and Gas 7 in the ischemic VPL of FCI rats may be involved in the neuroprotection and repairing; EA can significantly up-regulate the expressions of NGF and Gas 7 in VPL of the ischemic side, which may contribute to its effect in improving secondary thalamic impairment of FCI.

Effects of Polysaccharide of Gastrodia Elata Blume and Electro-Acupuncture on Expressions of Brain-Derived Neurotrophic Factor and Stem Cell Factor Protein in Caudate Putamen of Focal Cerebral Ischemia Rats.

BACKGROUND The aim of this study was to explore the neural protective effect of polysaccharide of Gastrodia elata Blume (PGB) and electro-acupuncture (EA) on focal cerebral ischemia rats. MATERIAL AND METHODS A total of 40 Sprague-Dawley rats were randomly divided into 5 groups (normal group, model group, PGB group, EA group and PGB+EA group). The model was prepared by middle cerebral artery occlusion (MCAO). Two week after modeling, rats were given PGB, EA, or a combination of the 2 in continuous treatment for 2 successive weeks. 14 days after modeling, expressions of BDNF and SCF protein in the caudate putamen (CPu) were detected by immunohistochemistry. RESULTS Positive expression of BDNF and SCF protein was found in the right caudate putamen of each group of rats. Expressions of BDNF and SCF in the CPu of the model group were higher than normal group (P<0.05). Compared with the model group, the expressions of BDNF and SCF in the CPu of the PGB group, the EA group, and the PGB plus EA group increased significantly (P<0.05). The expressions of BDNF and SCF obviously increased in the PGB plus EA group compared to those of the EA group and the PGB group (P<0.05). CONCLUSIONS PGB and EA up-regulated the expressions of BDNF and SCF protein in the CPu of focal cerebral ischemia rats, and the combination of PGB+EA has a synergistic effect on the recovery from cerebral ischemia.

[Effect of Electroacupuncture Combined with Polysaccharide of Gastrodia elata Blume on Ex- pression of Brain Derived Neurotrophic Factor and Vascular Endothelial Growth Factor in the Paraventricular Nucleus of Hypothalamus in Cerebral Ischemia Rat].

OBJECTIVE: To observe the effect of electroacupuncture(EA) of "Baihui" (GV 20) and "Zusanli" (ST 36) in combination with administration of polysaccharide of Gastrodia elata Blume (PGB) on the expression of brain derived neurotrophic factor (BDNF) and vascular endothelial growth factor(VEGF) in the paraventricular nucleus of hypothalamus(PVN) of cerebral ischemia (C) rats, so as to explore its mechanism underlying improvement of Cl. METHODS: Forty Sprague-Dawley rats were randomized into five groups: normal control, model, EA, PGB, and EA+ PGB (n = 8/group). The cerebral ischemia model was established by occlusion of the middle cerebral artery (MCAO). EA (2 Hz, 2 V) was applied to "Baihui" (GV 20) and "Zusanli" (ST 36) for 30 min, once daily for 14 days. The rats of the PGB and PGB+ EA groups were treated by intragastric gavage of PGB at a dose of 100 mg/kg, once daily for 14 successive days. The expression of BDNF and VEGF in the PVN of hypothalamus was detected by immunohistochemistry. RESULTS: After MCAO, the BDNF and VEGF immunoreactions (IR) positive neuron numbers and expression level in the PVN of the hypothalamus were significantly increased in the model group (P<0.05) and were further up-regulated after administration of EA and PBG ( P<0. 05). The effects of EA+ PGB were evidently superior to those of simple EA and simple PBG in up-regulating BDNF and VEGF IR-positive neuron numbers and expression levels in the PVN ( P<0.05). CONCLUSION: EA combined with PGB can up-regulate the expression of BDNF and VEGF in the PVN of hypothalamus in cerebral ischemia rats, which might contribute to its effect in improving cerebral ischemia.

[Effect of Electroacupuncture Intervention Combined with Gastrodin Administration on Neurological Function, Nogo-A and NgR Expression in the Frontal Lobe Cortex of Focal Cerebral Ischemia Rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention combined with medication (Gastrodin) on changes of neurological function and expression of Nogo-A and Nogo-A receptor (NgR) in the frontal lobe cortex around the ischemic loci of focal cerebral ischemia (FCI) rats, so as to explore its mechanism underlying improvement of neuroregeneration of FC. METHODS: Fifty male Sprague-Dawley rats were randomly divided into normal control, model, EA, medication and EA+ medication groups (n = 10 in each group). The FCI model was induced by occlusion of the middle cerebral artery (MCAO) with thread embolus. EA was applied to the left "Quchi" (LI 11) and "Hegu" (Li 4) for 30 min, once daily for 14 days after MCAO. For rats of the medication group, Gastrodin (10 mg/kg) was administrated by intraperitoneal injection, once daily for 14 days. The neurological impairment was assessed by Zea Longa's scoring. The expression of Nogo-A and NgR in the frontal lobe cortex around the ischemic loci was detected by immunohistochemistry. RESULTS: In comparison with the normal control group, cerebro- cortical Nogo-A and NgR expression levels of the model group vere significantly increased (P < 0.05). Compared with the model group, the Zea Longa's score and Nogo-A and NgR expression levels were evidently down-regulated in the EA, medication and EA + medication groups (P < 0.05). The Zea Longa's score and Nogo-A and NgR expression levels were significantly lower in the EA + medication group than in the EA and medication groups (P < 0.05). CONCLUSION: EA intervention and Gastrodin administration can down-regulate cerebro-cortical Nogo-A and NgR protein expression in FCI rats, which may contribute to their action in improving neurological impairment. The effect of EA+ Gastrodin is better than simple EA or Gastrodin treatment.

[Effect of Electroacupuncture plus Polysaccharide of Gastrodia elata Blume on Expression of Nestin and Brain Derived Neurotrophic Factor in the Basolateral Amygdala of Focal Cerebral Ischemia Rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) combined with administration of Polysaccharide of Gastrodia elata Blume (PGB) on stem cell proliferation in the basolateral amygdala (BLA) of focal cerebral ischemia (FCI) rats. METHODS: A total of 40 Sprague-Dawley rats were randomly divided into normal control,model,EA, PGB and EA+PGB groups (n=8 rats in each group). The FCI model was established by occlusion of the right middle cerebral artery. EA (2 Hz, 3 V) was applied to "Baihui" (GV 20) and the left "Zusanli"(ST 36) for 30 min, once daily for 14 successive days. Rats of the PGB and EA+PGB groups were given with PGB (100 mg/kg) by gastrogavage, once daily, for14 successive days. The Zea-Longa's method was used to determine the animals' nerurological dysfunction score on day 1 and 14. The expressions of Nestin and brain derived neurotrophic factor (BDNF) of the right BLA were measured by immunohistochemical staining. RESULTS: Following modeling, the neurological score, and the numbers of Nestin- and BDNF-immunoreaction (IR)-positive cells were significantly increased in the model group (P<0.05). Compared with the model group, the neurological scores were considerably decreased in the EA, PGB and EA+PGB groups (P<0.05), and the numbers of Nestin- and BDNF-IR positive cells were further significantly increased in the 3 treatment groups (P<0.05), and the effect of EA+PGB was notably superior to that of simple EA and simple PGB in down-regulating neurological score and up-regulating Nestin and BDNF expression (P<0.05). CONCLUSIONS: Both EA and PGB interventions can improve FCI rats' neurological function, which may be related to their effects in up-regulating the expression of Nestin and BDNF to promote the proliferation of neural stem cells in the BLA.

[Effects of electroacupuncture combined with polysaccharide of gastrodia elate blume on expression of nestin and stem cell factor in thalamic ventroposterolateral nucleus in rats with focal cerebral ischemia].

OBJECTIVE: To explore the nerve regeneration mechanism of electroacupuncture (EA) combined with polysaccharide of gastrodia elate blume (PGB) for secondary thalamic damage of focal cerebral ischemia. METHODS: Forty Sprague-Dawley adult rats were randomly divided into a normal control group, a model group, an EA group, a PGB group and an EA + PGB group, 8 rats in each group. The rat model of right middle cerebral artery occlusion was prepared by suture-occluded method. Two weeks after model establishment, rats in the normal control group and model group received no treatment; rats in the EA group were treated with EA at "Baihui" (GV 20) and left "Zusanli" (ST 36), 30 min per treatment, once a day for 14 successive days; rats in the PGB group were treated with intragastric administration of PGB (100 mg/kg) , once a day for 14 days; rats in the EA + PGB group were treated with EA and PGB treatment, once a day for totally 14 days. The expressions of nestin and stem cell factor (SCF) in thalamic ventroposterolateral nucleus (VPL) were detected by immunohistochemical method. RESULTS: There were positive cells of nestin in ischemia VPL in the model group, and the number of SCF positive cells was increased compared with that in the normal control group (P<0.05). The number of positive cells of nestin and SCF in ischemia VPL in the EA group, PGB group and the EA + PGB group was increased compared with that in the model group (all P<0.05), and the average gray value of immune positive product was all reduced (all P<0.05). The number of positive cells of nestin and SCF in the EA + PGB group was higher than that in the EA group or the PGB group (all P<0.05). CONCLUSION: EA combined with PGB can significantly increase the SCF expression in ischemia VPL and promote the proliferation of neural stem cells, which is likely to be one of the nerve regeneration mechanism of acupuncture and medication tor secondary thalamic damage of local cerebral isctemia.

[Effects of Electroacupuncture Intervention Combined with Gastrodin on Expression of Proteins Related to Proliferation-differentiation of Neural Stem Cells in Hippocampal CA 1 and CA 3 Regions in Focal Cerebral Ischemia Rats].

OBJECTIVE: To observe the effect of electroacupuncture(EA) combined with medication on changes of expression of Nestin, glial fibrillary acidic protein (GFAP) and neuron specific enolase (NSE) in the hippocampal CA 1 and CA 3 regions of focal cerebral ischemia (FC1) rats, so as to analyze its mechanisms underlying neuroprotection. METHODS: Fifty male SD rats were randomly divided into normal control, model, EA, medication, and EA+ medication groups (n = 10 in each group). The FCI model was established by middle cerebral artery occlusion (MCAO) with thread embolus. EA (2 Hz, 2 V) was applied to the left "Hegu"(LI 4) and "Quchi" (LI 11) for 30 min, once daily for 14 days after MCAO. Rats of the medication group were given with intraperitoneal injection of gastrodin (10 mg/kg). The expression of Nestin, GFAP and NSE in the hippocampal CA 1 and CA 3 regions were detected by immunohistochemistry. RESULTS: Compared with the normal control group, the numbers of Nestin- and GFAP-immunoreaction (IR) positive cells in both CA 1 and CA 3 regions of the hippocampus were significantly increased in the model ciroup (P<0.05), while those of NSE-IR positive cells in both CA 1 and CA 3 regions were significantly decreased in the mdlgroup (P<0.05). After EA and medication interventions, the numbers of Nestin- and NSE-IR positive cells in the CA 1 and CA 3 regions were evidently increased and GFAP-IR positive neurons were considerably reduced in the EA, medication and EA+ medication groups (P<0.05). The effects of EA+ medication were significantly superior to those of both EA and simple medication in up-regulating the number of Nestin- and NSE-IR positive cells and down-regulating the number of GFAP positive neurons in CA 1 and CA 3-regions (P<0.05). CONCLUSION: EA and EA intervention combined with gastrodin can significantly up-regulate the number of Nestin- and NSE-IR positive cells, and down-regulate the number of GFAP positive cells in the CA 1 and CA 3 regions of hippocampus in focal cerebral ischemia rats, which may contribute to their effects in promoting the differentiation and proliferation of mature neurons in the hippocampus for improving cerebral functions. The effects of EA+ medication are obviously better than simple EA intervention.

[Effects of electroacupuncture intervention combined with polysaccharide of Gastrodia elata Blume on expression of nestin and cytokines of neural stem cells in the dentate gyrus of cerebral ischemia rats].

OBJECTIVE: To observe the effect of electroacupuncture (EA) of "Baihui" (GV 20) and "Zusanli" (ST 36) and EA plus polysaccharide of Gastrodia elata Blume (PGB) on neural stem cell (NSC) proliferation in cerebral ischemia (CI) rats, so as to explore its mechanisms underlying improvement of CI. METHODS: A total of 40 SD rats were randomly divided into normal control, CI model, EA , medication (PGB) and EA + medication groups (n = 8 in each group). The CI model was established by occlusion of the middle cerebral artery (MCAO). Two weeks after modeling, rats of the medication and EA + medication groups were administrated with PGB (100 mg/kg) once daily for 2 successive weeks. EA (2 Hz, 3 V) was applied to "Baihui" (GV 20) and left "Zusanli" (ST 36) for 30 min, once daily for 2 weeks. The expression of Nestin and stem cell factor (SCF) proteins in the dentate gyrus (DG) of hippocampus was detected by immunohistochemistry. RESULTS: Compared with the normal control group, the expression of Nestin and SCF proteins in the suprapyramidal blade (SPB) and infrapyramidal blade (IPB) of DG were significantly increased in the model group (P < 0.05). After EA intervention, the expression levels of Nestin and SCF of SPB and IPB of DG were considerably further up-regulated in both EA group and EA + medication group (P < 0.05), and the effect of EA + medication group was significantly superior to that of simple EA group and medication group (P < 0.05). CONCLUSION: EA combined with PGB can significantly up-regulate the expression of Nestin and SCF in the hippocampal DG in CI rats, and its effects are apparently superior to those of simple EA or simple medication. It suggests that EA-induced proliferation of SCF may be one of the mechanisms underlying relieving CI.