The Baihui acupoint has three Yang and five convergences; it is needled in order to activate spirit and resuscitate the brain in traditional Chinese medicine. Therefore, the purpose of the present study is to investigate the effect of acupuncture stimulation at the Baihui acupoint on cerebral infarct and dopamine levels. A chronic cerebral hypoperfusion animal model was established by permanent ligation of both common carotid arteries; a cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and the right middle cerebral artery for 90 min followed by reperfusion in Sprague-Dawly (SD) rats. The Baihui acupoint was stimulated for 20 min 3 days per week for 4 weeks. The cognitive and memory functions were evaluated by measuring the successful rates for rats to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed; the dopamine levels in brain tissue were measured and the percentage of right to left hemisphere area was calculated. The results indicated that acupuncture stimulation (AS) did not increase the success rate of performing the 8-arm radial maze in chronic cerebral hypoperfusion and cerebral ischemia-reperfusion injured rat models. AS increased dopamine levels in the right cerebral cortex and hippocampus in the chronic cerebral hypoperfusion rats, and increased dopamine levels of the cerebral cortex in the cerebral ischemia-reperfusion injured rat's models. The neurological deficit score was similar between control and AS groups 24 hours after reperfusion, whereas the AS group comprised of ischemia-reperfusion injured rats had a greater percentage of right to left hemisphere area than the control group. In conclusion, AS at the Baihui acupoint for 4 weeks increased dopamine levels in the brain tissue of chronic cerebral hypoperfusion rats and of cerebral ischemia-reperfusion injured rats. The AS also reduced brain atrophy after cerebral infarct, suggesting that AS at the Baihui acupoint acts as neuroprotector. However, regular stimulation at the Baihui acupoint enhances cognition and memory functions need further study.
Panax Notoginseng Burk (PN) has been reported to improve blood circulation, as well as learning and memory functions. The purpose of the present study was to investigate the effect of PN on learning and memory functions in chronic cerebral infarct rats. A cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and right middle cerebral artery for 90 min followed by reperfusion for 4 weeks. PN (0.5 g/kg) was administered orally 3 days per week for 4 weeks, whereas the control group provided bait and water only. The learning and memory functions were estimated by measuring how successful rats were able to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed. The brains were sectioned and analyzed for ED1, glial fibrillary acid protein (GFAP), nuclear factor-kappaB, and brain derivative neurotrophin factor (BDNF) and beta-secretase by immunostaining. Cerebral infarct rats given PN were able to successfully navigate the 8-arm radial maze test four weeks after cerebral infarction. PN also increased ED1, BDNF and beta-secretase immunoreactive cells, but did not increase GFAP and NF-kappaB immunoreactive cells. PN attenuated the reduction in learning and memory functions induced by cerebral infarction in cerebral ischemia-reperfusion injured rats; it also increased the amount of activated microglia and BDNF. These data suggest that the effect of PN, at least in part, is closely related to the increase in BDNF that was generated by activated microglia. The effect that PN has on astrocytes, NF-kappaB and beta-secreatase immunoreactive cells requires further study.
Our previous studies showed that Gastrodia elata (GE), an herb used in traditional Chinese medicine, has both anti-convulsive and free radical-scavenging activities in kainic acid (KA)-treated rats. The aim of the present study was to further investigate possible physiological mechanisms of GE against activities of neuronal nitric oxide synthase (nNOS) and microglia in KA-treated rats; 0.5 g/kg and 1.0 g/kg of GE extract were administered orally, whereas 20 mg/kg of N-nitro-L-arginine methyl ester (L-NAME) was administered intraperitoneally (ip), both at 30 minutes prior to KA (2 microg/2 microl) being injected into the right hippocampus region of rats. ED1-staining, apoptotic, inducible nitric oxide synthase (iNOS), and nNOS-staining cells were observed in the hippocampus region. The results indicated that 1.0 g/kg of GE and 20 mg/kg of L-NAME reduced the counts of ED1-stained cells, and 0.5 g/kg and 1.0 g/kg of GE, and 20 mg/kg of L-NAME reduced the numbers of apoptotic cells and nNOS-staining cells. In addition, 20 mg/kg of L-NAME also reduced the numbers of iNOS-staining cells, but 0.5 g/kg and 1.0 g/kg of GE did not. This study demonstrated that GE was able to reduce nNOS, microglia activation and apoptosis, suggesting that GE has a protective effect against neuronal damage in KA-treated rats.
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