鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

鱼藤酮对中脑星形胶质细胞的损伤及阿糖胞苷的干预作用

Objective To observe the toxic effects of rotenone on the proliferation, γ-glutamylcysteinylglycine (GSH) content and the expression level of glial cell line-derived neurotrophic factor (GDNF) of rat rnidbrain astrocytes in vitro and the interventional effect of arabinoeytidine (ara-c). Methods In vitro cultured rat midbrain astrocytes were assigned randomly into 9 groups, including a normal control group, 4 short-term rotenone treatment groups exposed for 24 h to 10, 20, 40 or 60 nmol/L rotenone, 2 long-term rotenone treatment groups exposed for 30 days to 10 or 20 nmol/L rotenone, and 2 ara-c groups with 500 nmol/L ara-c treatment following exposure to 10 or 20 nmol/L rotenone for 6 days. The cell proliferation was assessed by immunocytochemical detection of the expression of proliferating cell nuclear antigen (PCNA). GSH content in the treated cells was measured by GSH detection kit, and the expression of GDNF was detected with immunocytochemistry and Western blot. Results The 24-h exposure to low-level rotenone (10 and 20 nmol/L) did not cause any changes in GSH content or GDNF expression in the cells. But at 40 and 60 nmol/L, rotenone treatment for 24 h significantly decreased the GSH content and GDNF expression. Rotenone exposure for 30 days increased the ratio of proliferating astrocytes and decreased GDNF expression level, but the GSH content remained stable. The application of 500 nmol/L ara-c to suppress the cell proliferation restored the expression level of GDNF to almost the control level and markedly increased GSH content. Conclusion Rotenone affects the proliferation and activity of rat midbrain astrocytes in vitro and deteriorates the microenvironment of dopaminergic neurons. Low-level ara-c can increase the GSH content and GDNF expression levels by suppressing the proliferation of rotenone-exposed astrocytes, suggesting its potential value in the treatment of Parkinson's disease.     

缺氧复氧大鼠海马星形胶质细胞凋亡及Bcl-2和Bax蛋白表达的时间进程变化及异丙酚干预效应

BACKGROUND： Cerebral hippocampal astrocytes are more sensitive.to ischemic injury than neurons. Hypoxic-ischemic brain injury induces profound astrocyte apoptosis, and propofol may protect against astrocyte apoptosis.
OBJECTIVE： To verify the protective effects of propofol against astrocyte apoptosis and to investigate anti-apoptotic Bcl-2 and pro-apoptotic Bax expression in primary cultures of rat hippocampal astrocytes exposed to hypoxia-reoxygenation for different periods of time following propofol treatment.
DESIGN, TIME, AND SETTING： In vitro neural immunocytochemistry was performed at the Central Laboratory of Yunyang Medical College between September 2007 and March 2008.
MATERIALS： A total of 30 Wistar rats, aged 1-3 days, wJth equal numbers of males and females, were included for isolation and culture of .hippocampal astrocytes.
METHODS： Hippocampal astrocytes were purified and cultured for 3 weeks and treated with four culture conditions： 50 μL Hank＇s solution （normal control）; 0.2 mL/L Intralipid; 50 μL Hank＇s solution for 10 minutes followed by hypoxic incubation for 4 hours and normoxic incubation for 12, 24, 36, 48, 60 or 72 hours; propofol （250 μmol/L final） for 10 minutes followed by hypoxic incubation for 4 hours and normoxic incubation for 12, 24, 36, 48, 60 and 72 hours.
MAIN OUTCOME MEASURES： （1） Morphologic changes in hippocampal astrocytes. （2） Levels of astrocyte apoptosis and Bcl-2 and Bax expression.
RESULTS： Hypoxia and reoxygenation increased apoptosis over time, with Bcl-2 expression peaking at 24 hours and decreasing gradually （P 〈 0.01 ）; Bax expression peaked at 72 hours （P 〈 0.01）; the ratio of Bcl-2/Bax was 1.4, 0.8, and 0.6, respectively, at 24, 48 and 72 hours. Non-apoptotic astrocytes showed significant proliferation and swelling. Propofol treatment decreased apoptosis after hypoxia-reoxygenation （P 〈 0.01）, as well as Bct-2 and Bax expression （P 〈 0.05, P 〈 0.01）, with Bcl-2/Bax ratios of 1.6-1.8. Propofol treatmentalso blocked astrocyte proliferation and swelling. No apoptotic cells or Bcl-2/Bax expression was detected in astrocytes cultured in Hank＇s or Intralipid solution.
CONCLUSION： Propofol protects astrocytes against injury caused by hypoxia and reoxygenation via a mechanism that involves maintaining high ratios of Bcl-2/Bax.     

电针对局灶性脑缺血大鼠缺血灶周围区星形胶质细胞的影响

BACKGROUND： Astrocytes react sensitively to cerebral ischemia, causing reactive proliferation and activation, which may contribute to their effect in protecting or injuring neuronal regeneration. Whether acupuncture, as a treatment for cerebral ischemia, regulates the activated state of astrocytes has become a focus of recent investigations. OBJECTIVE： To observe the effects of electroacupuncture （EA） on ultrastructure changes and reactive proliferation of astrocytes in the marginal zone of focal cerebral ischemia in rats. DESIGN, TIME AND SETTING： Randomized, controlled animal study. This study was performed at the Experimental Animal Center of Guangzhou University of Traditional Chinese Medicine between December 2007 and July 2008. MATERIALS： A total of 90 male Wistar rats were randomly divided into sham operated, model and EA groups. Each group was subdivided into 1 hour, 1, 3, 7, and 21 days post-cerebral ischemia groups, with six animals for each time point. Rabbit anti-rat glial fibrillary acidic protein （GFAP） and goat anti-rabbit IgG/tetramethylrhodamine isothiocyanate were provided by Beijing Biosynthesis Biotechnology. The G-6805 electric acupuncture apparatus was provided by Shanghai Huayi. METHODS： Heat-coagulation-induced occlusion of the middle cerebral artery was performed to establish a model of focal cerebral ischemia, in the model and EA groups. Middle cerebral arteries were exposed without occlusion in sham operated group. EA was applied immediately after surgery in the EA group, 4/20 Hz, 2.0-3.0 V, 1-3 mA, to Baihui（GV 20） and Dazhui（GV 14）, for 30 minutes. The treatment was performed once a day. The sham operated and model groups did not receive acupuncture. MAIN OUTCOME MEASURES： In the marginal zone of focal cerebral ischemia in rats at different time points after intervention, the ultrastructure changes of astrocytes were observed by using transmission electronic microscopy. GFAP expression in astrocytes was also measured by laser confocal scanning microscopy. RESULTS： Cell swelling and rapid proliferation of astrocytes were observed following cerebral ischemia. In comparison to the model group, the degree of swelling of astrocytes was significantly decreased in the EA group. Compared with the sham operated group at hour 1 post-surgery, there was no significant difference in the expression of average fluorescence intensity of GFAP between the EA and model groups （P 〉 0.05）, while the expression of GFAP in both the EA and model groups increased significantly at days 1, 3, 7 and 21 post-surgery （P 〈 0.01）. The expression of GFAP in EA group was also significantly lower than in the model group （P 〈 0.01, P 〈 0.05）. CONCLUSION： Ultrastructural changes and reactive proliferation of astrocytes appear in the marginal zone of focal cerebral ischemia in rats. EA can relieve the degree of swelling of astrocytes and inhibit GFAP overexpression by activated astrocytes. These effects may be related to its ability to regulate the activated state of astrocytes.     

Mental illness in England,in Scotland and in Scots living in England

Summary Beginning from the observation that Scots living in England have much higher rates of mental hospital admission than do the English, several hypotheses are proposed to account for this. Much of the excess in rates of mental illness is accounted for by those diagnosed as having alcohol-related disorders and behaviour and personality problems. The results of an examination of offical statistics in the two countries enabled some explanations to be offered. It was found that rates of admissions to mental hospitals are higher in Scotland than in England but not as high as those found among Scots migrants who have a much higher rate of readmission to hospitals than either of the other groups. In fact, if first admissions only are considered the rates of admission in Scotland are not only higher than rates for English natives but also higher than for Scottish migrants. It seems that Scots living in England are somewhat less likely to become mental patients than Scots in Scotland but that once they do achieve this status they are very much more likely to be readmitted on subsequent occasions. It was concluded that there might be two fairly distinct groups of migrants from Scotland to England who have different backgrounds, different reasons for migrating and different psychological characteristics. On the one hand there are stable, economically motivated migrants who move south for definite employment related reasons and who show few psychological symptoms. While on the other hand there is a group of migrants who perhaps have psychological problems and who move more in hope than expectation without definite prospects and who account for the high rates of mental hospital admission found in Scottish migrants.     

Prostacyclin release in the coronary circulation during sustained stimulation in in vitro and in in vivo experimental systems

Prostacyclin release from rat isolated perfused hearts and from dog coronary circulation was studied by measuring immunoreactive 6-keto-PGF1 alpha (6-keto-PGF1a) in heart perfusate and in plasma obtained from the great cardiac vein respectively. Continuous infusion of arachidonic acid at constant concentration in isolated perfused hearts induced an increased prostacyclin release. This release showed a rapid peak within 10 min and a subsequent decrease. Low-flow ischemia induced an increased perfusate concentration of 6-keto-PGF1a but, considering the decreased flow, prostacyclin release was actually reduced. During the whole period of ischemia (60 min) prostacyclin release was constant. In open-chest anesthetized dogs 6-keto-PGF1a concentration in the great cardiac vein was increased after ligation of the left anterior descending coronary artery. A prolonged period of coronary occlusion (4.5 hours) resulted in a progressive rise of prostacyclin release. 6-keto-PGF1a determinations in the femoral vein and in the aorta did not show relevant variations during the observation period.     

癫痫与抑郁关系的研究进展

抑郁是癫痫患者中常见的精神障碍,严重地影响了患者的生活质量。传统的观点认为癫痫患者因为存在着诸多社会学问题易出现抑郁倾向,癫痫和抑郁是单向的联系,但大量的研究已经证明癫痫和抑郁之间存在双向的联系,一种异常状态的存在可能易转化为另一种异常状态的发展。癫痫和抑郁存在着共同的发病机制。本文主要就癫痫和抑郁的双向联系以及抗抑郁药物在癫痫患者中的应用进行阐述。     

神经介入：回眸2022

<正>2022年,国际上公布了多项大型神经介入领域的随机对照试验（randomized controlled trial,RCT）结果,在血管内治疗（endovascular treatment,EVT）急性大血管闭塞（large vessel occlusion,LVO）适应证的扩展、药物治疗、管理,症状性颅内动脉粥样硬化性狭窄（symptomatic intracranial atherosclerotic stenosis,sICAS）治疗,无症状性颈动脉狭窄治疗,     

Neuroimaging in epilepsy in tropics

Epilepsy is a major public health problem in many tropical countries. Also, some of the tropical diseases are major contributors to the higher prevalence of epilepsy in these countries. The etiologic factors responsible for epilepsy in these countries are quite different from those in the developed world. This article discusses the etiologic factors and neuroimaging of epilepsy in light of the conditions in these tropical countries.