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Objective: To observe the effects of electroacupuncture (EA) with three frequencies (100 Hz, 2 Hz, and 2 Hz/100 Hz) on the apoptosis of neurons and c-Jun N-terminal kinase (JNK) signaling pathway in the hippocampus of rats with vascular dementia (VD), and explore the mechanism of EA intervention for VD. Methods: Fifty male Sprague-Dawley rats were randomly divided into a model group, a sham operation group, a 100 Hz EA group, a 2 Hz EA group, and a 2 Hz/100 Hz EA group, with ten rats in each group. The VD model rats were established by repeated ischemia-reperfusion of bilateral common carotid arteries. The rats in the EA groups received EA intervention at Baihui (GV20), Dazhui (GV14), Geshu (BL17) and Zusanli (ST36), once a day for 14 d. Afterward, Morris water maze was used to examine the learning and memory performances of the rats in each group, hematoxylin-eosin staining to observe the histomorphological changes in the hippocampal CA1 region, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling to test the apoptosis of neurons in the hippocampal CA1 region, and Western blot to detect the protein expression levels of JNK, phosphorylated JNK (p-JNK), Caspase-8, and Caspase-3 in the hippocampus tissue. Results: Compared with the sham operation group, the escape latency of the model group in water maze test was prolonged; the number of crossing the original platform was decreased (P<0.01); the hippocampal neurons were severely damaged and the number of surviving neurons was decreased (P<0.01), whereas the number of apoptotic neurons was increased (P<0.01); the protein expression levels of JNK, p-JNK, Caspase-8, and Caspase-3 in the hippocampus were significantly increased (P<0.01). Compared with the model group, the escape latency of each EA group was significantly shortened; the number of crossing the original platform was significantly increased (P<0.01); the damage of hippocampal neurons was alleviated, the number of surviving neurons was increased (P<0.01), and the number of apoptotic neurons was decreased (P<0.01); the protein expression levels of JNK, p-JNK, Caspase-8, and Caspase-3 in the hippocampus were decreased (P<0.01). The results in the 2 Hz EA group and the 2 Hz/100 Hz EA group were superior to those in the 100 Hz EA group. Conclusion: EA with the three frequencies (100 Hz, 2 Hz, and 2 Hz/100 Hz) can improve the learning and memory performances in VD rats subjected to ischemia-reperfusion, its mechanism may be related to the inhibition of neuronal apoptosis and the regulation of the related protein expression of JNK signaling pathway, and the intervention effects of EA with 2 Hz and 2 Hz/100 Hz are more significant.
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Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
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Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
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Autophagy is a process of degrading the damaged organelles and macromolecules by lysosomes in cells, which belongs to the programmed cell death. Cerebral ischemia is one of the important reasons for activation of autophagy. Studies have showed that autophagy plays a protective role in neuronal death induced by ischemia. However, it has also been found that excessive activation of autophagy could aggravate cerebral ischemia injury. In recent years, more and more Chinese medicine has been proved to regulate the autophagy level of brain neurons and reduce cerebral ischemia injury. In this paper, the main molecular mechanism of autophagy in the process of cerebral ischemic injury and the intervention effects of Chinese herbs on autophagy arereviewed in order to explore the basic principle of regulating autophagy by Chinese herbs and to play a better role in the clinical treatment of cerebral ischemic diseases.
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Objective: To observe the effect of traditional Chinese medicine Jiusuyu(酒速愈) on activities of superoxide dismutase(SOD) and catalase(CAT),as well as the content of malondialdehyde(MDA) in liver tissues of mice with acute alcoholism.Methods: The models of acute alcoholism mice were established by drinking 56% Hongxing Erguotou(红星二锅头) drink.Eighty healthy Kunming mice were randomly divided(into) normal group,model group,high Jiusuyu dosage group,low Jiusuyiu dosage group and Gehua Jiecheng decoction(葛花解酲汤) group,with 16 animals in each group.The SOD,CAT activities and the content of MDA in(liver) tissues of each group were detected 6 hours after treatment.Results: The content of MDA in(liver) tissues of the model group was increased(P
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BACKGROUND: The onset of vascular dementia (VD) is closely related to brain ischemic-hypoxia. Previous research has proved that behavioral disturbance can be obviously attenuated by xingnao qizhi capsule in VD rats; however, it remains unclear whether the improvement of VD is due to the protection on ischemic cells.OBJECTIVE: Pheochromocytoma PC12 cells were cultured in vitro and exposed to Na2S2O4 to induce hypoxia injury. Then serum pharmacological technique was used to investigate the protection of xingnao qizhi drug serum on hypoxia-injured PC12 cells.DESIGN: Randomized controlled study.SETTING: School of Traditional Chinese Medicine of Hebei Medical College.PARTICIPANTS: This study was conduced at the Experimental Animal Laboratory and Cell Culture Laboratory, School of Traditional Chinese Medicine of Hebei Medical College, between June and December 2003.Forty SD rats were randomized into 5 groups, namely serum control group (n=12) and xingnao qizhi serum 25.42, 12.71, 6.35 and 3.18 g/kg groups (n=7). PC12 cell line was purchased form the Cell Center of Chinese Academy of Medical Sciences.serum 25.42, 12.71, 6.35 and 3.18 g/kg groups were exposed through gastric lavage to xingnao qizhi of corresponding dosages (composed of wolfberwhile normal saline was given by gastric lavage to rats in control group in dosage of 10 mL/kg, twice a day at an interval of 12 hours for 3 consecutive days. One hour after the last administration, femoral blood samples were collected when rats were deeply anaesthetized and serum was sepainto 6 groups. Cells in control group were cultured with control serum while in experimental model groups cells were exposed to Na2S2O4 to induce hypoxia injury 1 hour later. Cells in Xingnao Qizhi 25.42, 12.71,6.35 and 3.18 g/kg groups were cultured in 5% drug serum with corresponding dosage of xingnao qizhi drug for 1 hour before being exposed to changes of PC12 cells in the six groups were observed under reversal microscope after exposure to Na2S2O4 for 16 hours; the inhibition rate of lactate dehydrogenase production and PC12 cell injury (MTT method) was calculated for assessing cell activity.nase production and PC12 cell injury.of xingnao qizhi displayed better refraction, with fewer cell fragments that tion: It was 81.6%, 69.6%, 54.4% and 27.8% in xingnao qizhi 25.42,PC12 cell injury: It was 82.9%, 75.6%, 65.9% and 53.7% in Xingnao Qizhi 25.42, 12.71, 6.35 and 3.18 g/kg groups, respectively.CONCLUSION: xingnao qizhi drug serum can markedly attenuate hypoxia injury of PC12 cells in dose-dependant manner, which is presented by strengthened cell activity and decreased lactate dehydrogenase activity.