Protective effects of soybean phospholipid liposome on glutamate-induced nerve cell injury in vitro

BACKGROUND: It has been previously reported that soybean phosphatide could reduce the cerebral ischemia damage obviously. Whether soybean phospholipid liposome (SPL) can protect cerebral cortical neurons cultured in vitro from glutamate (Glu)-induced neurotoxicity, particularly nerve cell membrane damage has not been fully investigated. OBJECTIVE: To study the protective effects of SPL on Glu-induced neurotoxicity of neurons in culture, and to discuss the possible mechanisms of neuroprotection. DESIGN: Randomized controlled trial. SETTING: Department of Biochemistry, Liaoning Medical University. MATERIALS: Twelve Sprague-Dawley rats, of either gender, aged 0 to 1 day, were involved in this study. Drugs and reagents: poly-L-lysine and L-glutamate were purchased from Sigma company (USA). METHODS: The study was carried out in the Department of Biochemistry of Jinzhou Medical University from November 2004 to June 2005. Glu（1×10–4 mol/L）was added to cortical neurons in injury group for 3 hours, while different concentrations of SPL (0.2, 0.4, 0.8, 1.6 g/L) were added at the same time in the SPL groups. Neurons in the normal control group were untouched. MAIN OUTCOME MEASURES: According to the instruction of reagent kit, lactate dehydrogenase(LDH) activity and nitric oxide(NO) content in the supernatant fluid of the culture medium were assayed, and the activity of nitric oxide synthase (NOS) and superoxide dismutase(SOD), malonaldehyde (MDA) content in the neurocytes were also determined. RESULTS: ①Activities of LDH and NOS, as well as NO content in the supernatant fluid of injury group were significantly higher than those of normal control group (P < 0.01). Activities of LDH and NOS, and NO content in the supernatant fluid of SPL groups were significantly lower than those of injury group (P < 0.01). ②MDA content of the SPL groups was significantly lower than that of injury group (P < 0.01); SOD activity of neurons in the injury group was significantly lower than that in the normal control group (P < 0.01), but was significantly higher than that in the injury group (P < 0.01). ③ The protective effect of SPL increased with increasing concentration (0.2–0.8 g/L), and plateaus at around 1.6 g/L. CONCLUSION: SPL can protect rat cerebral cortical neurons from Glu-induced neurotoxicity in a dose-dependent manner. This protection is possibly related to SPL's effect against damages associated with lipid peroxidation.     

Effects of epigallocatechin gallate on rotenone-injured murine brain cultures

Green tea polyphenol epigallocatechin-3-gallate (EGCG) is reported to have antioxidant abilities and to counteract beneficially mitochondrial impairment and oxidative stress. The present study was designed to investigate neuroprotective effects of EGCG on rotenone-treated dissociated mesencephalic cultures and organotypic striatal cultures. Rotenone is a potent inhibitor of complex I of the respiratory chain, which in vitro causes pathological and neurochemical characteristics of diseases in which mitochondrial impairment is involved, e.g., Parkinson’s disease. Treatment with EGCG (0.1, 1, 10 μM) alone had no significant effects on mesencephalic cultures. In striatal slice cultures, EGCG led to a significant increase of propidium iodide (PI) uptake and 4-amino-5-methylamino-2′,7′-difluorofluorescein diacetate (DAF-FM), but not dihydroethidium (DHE) fluorescence intensity. Rotenone (20 nM on the eighth DIV for 48 h) significantly decreased the numbers and the neurite lengths of TH ir neurons by 23 and 34% in dissociated mesencephalic cell cultures compared to untreated controls. Exposure of striatal slices to rotenone (0.5 mM for 48 h) significantly increased PI uptake, and DAF-FM and DHE fluorescence intensities by 41 and 136 and 19%, respectively, compared to controls. Against rotenone, in dissociated mesencephalic cultures, EGCG produced no significant effect on either the number or neurite lengths of THir neurons compared to rotenone-treated cultures, but EGCG significantly decreased PI uptake by 19% and DAF-FM fluorescence intensity by 19 and 58%, respectively, compared to increase in rotenone-exposed striatal slices. On the other hand, EGCG did not affect superoxide (O₂ ⁻) formation as detected with DHE. These data indicate that EGCG slightly protects striatal slices by counteracting nitric oxide (NO^·) production by rotenone. In conclusion, EGCG partially protects striatal slices but not dissociated cells against rotenone toxicity.     

黄芪的抗神经细胞缺氧损伤作用

目的观察黄芪抗神经细胞缺氧损伤的作用。方法用氰化钠造成体外培养新生大鼠大脑皮层神经细胞缺氧模型，比较黄芪组和对照组的细胞形态、存活细胞数（四唑盐微量自动比色检测Ａ值）、乳酸脱氢酶（ＬＤＨ）值和钾离子（Ｋ＋）流出的变化。结果缺氧４８小时后，对照组Ａ值由缺氧前的０３２５±００３１降至０１４５±００１１，ＬＤＨ和Ｋ＋漏出量分别由６５８０±２９０Ｕ／Ｌ、５２３±０１１ｍｍｏｌ／Ｌ增至１４８８０±８４０Ｕ／Ｌ、７３１±０１８ｍｍｏｌ／Ｌ。而此时黄芪组Ａ值为０１７８±００１１、ＬＤＨ漏出量为１２７２５±７８４Ｕ／Ｌ，Ｋ＋含量为６９３±０１５ｍｍｏｌ／Ｌ。与对照组相比，黄芪组受损程度明显减轻。结论黄芪具有一定的抗神经细胞缺氧损伤作用     

促红细胞生成素对大鼠脑损伤后神经保护作用的实验研究

目的探讨促红细胞生成素(EPO)对颅脑损伤后的神经保护作用。方法成年SD大鼠55只,随机分为假手术组(n=5)、对照组(n=25)和EPO治疗组(n=25);对照组和治疗组采用改进的Feeney等人的方法制作脑创伤模型,根据伤后处理时间点每组再分为5个亚组,即伤后6h、24h、48h、72h和168h组,每亚组5只动物。检测各组动物在EPO处理前后不同时间点神经行为评分和脑含水量变化;放射免疫法检测肿瘤坏死因子(TNF-α)与白介素-1β(IL-1β)的水平。结果与对照组相比,在脑损伤后24～48hEPO治疗组神经行为评分明显增加(P0.05),在伤后48～168h脑含水量明显降低(P0.05)。在颅脑损伤后6～168hEPO治疗组血清TNF-α含量明显低于对照组(P0.05),而血清IL-1β的含量在伤后24～168hEPO治疗组也明显低于对照组(P0.05)。结论本研究提示EPO对大鼠脑损伤后的神经有保护作用。     

Neurotoxic effects of aluminium on embryonic chick brain cultures

Toxic damage of brain cells by aluminium (A1) is discussed as a possible factor in the development of neurodegenerative disorders in humans. To investigate neurotoxic effects of A1, serum-free cultures of mechanically dissociated embryonic chick (stage 28–29) forebrain, brain stem and optic tectum, and for comparison meningeal cells, were treated with A1 (0–1000 M) for 7 days. Effects of A1 on cell viability (lysosomal and mitochondrial activity) and differentiation (synthesis of cell-specific proteins) were found to the brain area specific with the highest sensitivity observed in optic tectum. No inhibiting effects on cell viability could be observed in cultures of forebrain and meninges in the concentration range tested. In all three brain tissue cultures, threshold levels for the reduction of cell differentiation parameters were found at lower concentrations [concentration resulting in a 50% decrease (IC₅₀)>180 M] than for the inhibitionof cell viability (IC₅₀>280 M) indicating a specific toxic potential of A1 for cytoskeletal alterations. The culture levels of nerve cellspecific markers microtubule-associated protein type 2 (the most sensitive parameter) and the 68-kDa neurofilament were inhibited at lower concentrations (IC₅₀ 180–630 M) than the astrocyte-specific glial fibrillary acidic protein (IC₅₀ 700–1000 M), demonstrating a particularly high sensitivity of neurons in comparison to astrocytes. Based on these differences in A1 sensitivity observed for different cell markers in the various brain tissue cultures, the in vitro system used in the present study proved to be a suitable model to assess brain area and cell type-specific neurotoxic effects of A1.This study is part of the Ph. D. thesis of Judith P. Mueller.Preliminary results were presented at the 24th Annual Meeting of the Swiss Societies for Experimental Biology (USGEB/USSBE)     

Neuroprotective effect of docosahexaenoic acid on glutamate-induced cytotoxicity in rat hippocampal cultures

The neuroprotective effect of docosahexaenoic acid (DHA) on the glutamate-induced cytotoxicity in rat hippocampal cultures was investigated in the present study. DHA at 5-50 microg/ml successfully protected neurons against the cytotoxicity, markedly increased the cell viability, inhibited both nitric oxide (NO) production and calcium influx, and increased the activities of antioxidant enzymes of glutathione peroxidase (GSH-Px) and glutathione reductase (GR). However, it did not alter the levels of glutathione (GSH) as compared to the control. These results suggest that DHA might be a potent neuroprotector. In addition, they may help to improve our understanding of the effect of DHA on neurodegeneration.     

Protective function of taurine in glutamate-induced apoptosis in cultured neurons

Previously, we showed that taurine protects neurons against glutamate-induced excitotoxicity by inhibiting the glutamate-induced increase of [Ca2+](i). In this study, we report that taurine prevents glutamate-induced chromosomal condensation, indicating that taurine inhibits glutamate-induced apoptosis. We found that Bcl-2 was down-regulated while Bax was up-regulated by glutamate treatment, and these changes were prevented in the presence of taurine. We have also shown that taurine inhibits glutamate-induced activation of calpain. Furthermore, calpastatin, a specific calpain inhibitor, also prevented glutamate-induced cell death. Here we propose the mechanisms underlying glutamate-induced apoptosis and taurine's inhibition of glutamate-induced apoptosis to be as follows: glutamate stimulation induces [Ca2+](i) elevation, which in turn activates calpain; activation of calpain leads to a reduction of Bcl-2:Bax ratios; with decreased Bcl-2:Bax ratios Bax homodimers form, Bax homodimerization, and translocation to the mitochondria result in the release of cytochrome c; released cytochrome c in turn activates a downstream caspase cascade leading to apoptosis. The antiapoptotic function of taurine is due to its inhibition of glutamate-induced membrane depolarization.     

葡多酚对实验性慢性酒精中毒的脑保护作用

目的 通过建立一种新型、稳定的大鼠慢性酒精中毒模型,探讨慢性酒精中毒的脑损伤机制以及葡多酚的抗氧化作用.方法 采用逐渐增加酒精浓度的自由饮用方式制成慢性酒精中毒模型.将250～300g成年Wistar大鼠随机分为4组:即对照组、多酚组、乙醇组和治疗组.测量大鼠体重;检测大鼠记忆功能;观察脑组织HE染色变化以及神经元凋亡情况.结果 本实验模型稳定性好、成模率高、死亡率低、重复性好、操作简便.乙醇组体重增长缓慢并伴有一过性负增长,明显的记忆功能障碍;而治疗组体重增加较好,未出现记忆功能减退.乙醇组饮酒时间越长,病理改变越明显;治疗组病理改变明显轻于乙醇组.乙醇组与对照组相比bcl-2和bax呈现升高的变化趋势,治疗组与乙醇组bcl-2/bax的比例无明显差别.结论 采用逐渐增加酒精浓度的自由饮用方式可成功建立理想的慢性酒精中毒模型;慢性酒精中毒可导致进行性记忆功能障碍、神经元坏死;葡多酚可明显减轻慢性酒精中毒引起的大鼠营养障碍、记忆功能减退和神经元坏死.     

Serum prevents glutamate-induced mitochondrial calcium accumulation in primary neuronal cultures

The effect of serum proteins on glutamate-induced mitochondrial calcium accumulation was studied in primary cortical and hippocampal cultures using oxalate-pyroantimonate staining with electron microscopy. Cultures were prepared from rat embryos on gestational day 17–19 and cultivated for 8 days in minimal essential medium (MEM) containing 5% native horse serum. At this time cultures were exposed for 5 min to 100 μM or 1.0 mM glutamate, followed by recovery in either serum-free or serum-containing culture medium. Mitochondrial calcium accumulation was assessed before glutamate treatment, at the end of glutamate exposure, and after 5 min, 30 min, 6 h and 24 h of recovery. Under control conditions and at the end of glutamate exposure, mitochondria contained only a few calcium deposits. If cultures were placed in serum-free medium after glutamate treatment, mitochondria were progressively loaded with calcium. At 5 min after glutamate exposure mitochondrial calcium deposits were prominent in both cortical and hippocampal cultures, followed by a further steady increase and neuronal death within 24 h. When cultures were allowed to recover after glutamate treatment in serum-containing MEM, calcium sequestration and ultrastructural changes of mitochondria were essentially absent, and neurons survived. No differences between cortical and hippocampal cultures were observed. The data demonstrate that prevention of glutamate neurotoxicity by serum proteins is associated with prevention of post-glutamate mitochondrial calcium accumulation. Received: 21 December 1995 / Revised, accepted: 25 March 1996     

Bunazosin hydrochloride reduces glutamate-induced neurotoxicity in rat primary retinal cultures

To study neuroprotective effects of bunazosin hydrochloride which is an alpha(1)-adrenoceptor antagonist used as an ocular hypotensive drug compared to other alpha(1)-adrenoceptor antagonists, and its mechanism of action. We evaluated the neuroprotective effects of bunazosin hydrochloride or seven other alpha(1)-adrenoceptor antagonists against glutamate-induced cell death in rat primary retinal cultures. We also evaluated the binding inhibition of bunazosin hydrochloride for 24 different receptors/channels and its effects on the Na(+) influx into cells induced by veratridine or glutamate. Bunazosin hydrochloride significantly inhibited glutamate-induced cell death at concentrations of 1 and 10 microM. Cells were also protected when treated with some alpha(1)-adrenoceptor antagonists, but not by the others. Bunazosin hydrochloride showed a high inhibition for Na(+) channels and inhibited the Na(+) influx induced by veratridine or glutamate. These findings indicate that in retinal cultures bunazosin hydrochloride has a neuroprotective effect against glutamate-induced cell death and that the inhibition of Na(+) channels by bunazosin hydrochloride may be partly responsible for this effect.     

Protective effects of liposome-entrapped superoxide dismutase on posttraumatic brain edema

Oxygen-derived free radicals and membrane lipid peroxidation have been postulated to be involved in brain edema and cell death, secondary to ischemia and traumatic injury. Using a model of brain edema induced by cold-induced injury, we have demonstrated an early elevation of superoxide radicals followed by permeability changes in the blood-brain barrier and development of edema in injured brain. Intravenous injection of liposome-entrapped copper-zinc-superoxide dismutase 5 minutes before the injury-enhanced entry of the enzyme into endothelial cells of the blood-brain barrier of injured brain reduced the brain level of superoxide radicals and ameliorated blood-brain barrier permeability changes and brain edema. Identical treatment 5 minutes after injury was also effective. These data demonstrate that superoxide radicals play an important role in the delayed development of vasogenic brain edema following brain injury.     

乌司他丁对创伤性脑损伤的保护作用研究

目的探讨乌司他丁(UTI)对创伤性脑损伤的保护作用和具体机制。方法 BALB/c小鼠27只,随机分为空白组(shame组)、生理盐水对照组(control组)、损伤组(TBI组)和乌司他丁预处理组(UTI组)。利用小鼠神经功能评分(NSS)法判断乌司他丁的治疗作用;Western blot方法检测脑组织中cathepsin B蛋白表达变化情况。结果与shame组比较,TBI组的cathepsin B蛋白表达明显增加(P<0.05),UTI组cathepsin B蛋白表达显著减少(P<0.05);与空白组比较,UTI组能明显减轻神经功能障碍,各组间差异有统计学意义(P<0.05)。结论乌司他丁预处理可能通过调控cathepsin B减轻细胞死亡,从而有效改善脑损伤后神经功能,具有显著的神经保护作用。     

Protective effect of resveratrol against oxygen-glucose deprivation in organotypic hippocampal slice cultures: Involvement of PI3-K pathway

Here we investigated the neuroprotective effect of resveratrol in an in vitro model of ischemia. We used organotypic hippocampal cultures exposed to oxygen-glucose deprivation (OGD). In OGD-vehicle exposed cultures, about 46% of the hippocampus was labeled with PI, indicating a robust percentage of cell death. When cultures were treated with resveratrol 10, 25 and 50 microM, the cell death was reduced to 22, 20 and 13% respectively. To elucidate a possible mechanism by which resveratrol exerts its neuroprotective effect, we investigated the phosphoinositide3-kinase (PI3-k) pathway using LY294002 (5 microM) and mitogen-activated protein kinase (MAPK) using PD98059 (20 microM). The resveratrol (50 microM) neuroprotection was prevented by LY294002 but was not by PD98059. Immunoblotting revealed that resveratrol 50 microM induced the phosphorylation/activation of Akt and extracellular signal-regulated kinase-1 and -2 (ERK1/2) and the phosphorylation/inactivation of glycogen synthase kinase-3beta (GSK-3beta). Our results suggest that PI3-k/Akt pathway are involved in the neuroprotective effect of resveratrol.     

Transferrin, carbonic anhydrase C and ferritin in dissociated murine brain cell cultures

It is shown here that transferrin (Tf), the iron transport protein and carbonic anhydrase C (CA C) are specifically located within oligodendrocytes in murine brain cell cultures. Ferritin (F), the major iron storage protein, was demonstrated in oligodendrocytes, as well as in astrocytes and microglial cells and was more prominent in the former. CA C and Tf were seen first after 6-7 days in culture. CA C and F positivity increased rapidly and at day 20, 80-85% of galactocerebroside + oligodendrocytes were positive for both proteins. Only a small number of oligodendrocytes was Tf+ up to day 14, after which their numbers increased rapidly until day 20, when 67% of the oligodendrocytes were Tf+. Because of the presence of Tf and F in oligodendrocytes it is suggested that these cells may play an important role in the metabolism of iron within the central nervous system.     

Iridoids from Scrophularia buergeriana attenuate glutamate-induced neurotoxicity in rat cortical cultures

In previous work, we isolated 7 neuroprotective iridoid glycosides from the 90% MeOH fraction of Scrophularia buergeriana (Scrophulariaceae). We therefore investigated the mode of action of 8-O-E-p-methoxycinnamoyl-harpagide (8-MCA-Harp), the most potent neuroprotective iridoid, and its aglycone, harpagide (Harp) using primary cultures of rat cortical cells in vitro. 8-MCA-Harp only revealed its neuroprotective activity in a pretreatment paradigm; this iridoid had more selectivity in protecting neurons against N-methyl-D-aspartate (NMDA)-induced neurotoxicity as opposed to that induced by kainic acid (KA). On the other hand, Harp exerted significant neuroprotective activity when it was administered either before or after glutamate insult and protected cultured neuronal cells from neurotoxicity induced by NMDA or KA. Furthermore, Harp significantly prevented the decrease of glutathione, an antioxidative compound in the brain, in our cultures. Finally, 8-MCA-Harp and Harp could successfully reduce the overproduction of nitric oxide and the level of cellular peroxide in cultured neurons. Collectively, these results suggested that Harp and 8-MCA-Harp protected primary cultured neurons against glutamate-induced oxidative stress primarily by acting on the antioxidative defense system and on glutamatergic receptors, respectively.     

Protective elements in traditional cultures

Among the environmental factors which have to be taken into account by psychiatric epidemiologists, when trying to interpret differences in the prevalence of neurotic and psychosomatic symptoms in different populations, the influence of social support systems is frequently invoked. For example, the pioneer community surveys carried out by Alex Leighton and his co-workers in Nova Scotia and in Nigeria showed that groups of people living in areas which exhibited features of social disintegration presented significant increases in the prevalence rates for such symptoms. Leighton also showed that in town-dwelling Nigerians, contrary to the findings in most other surveys, men showed higher rates of symptoms than women. He argued that in situations of rapid economic, occupational and social change the men of this population experienced more radical changes in their life-style than did the women, and attributed the women's lower rates to the assurance given to them by the continuance of their important domestic and child-rearing roles.In many other surveys, in Taiwan, Ethiopia and India it has been shown that symptom rates are higher, for both men and women, among those who have recently moved from rural to urban surroundings. This finding recalls Durkheim's observation of the loss of $\text{solidarite}$, and development of $\text{anomie}$ among French villagers who moved into the industrial towns of France, a hundred years ago.A more specific illustrate of the consequence of losing an important elemetn in a long-established social support system was provided by the findings of a symptom-prevalence survey carried out among villagers in a rural area of South India by Dr. R.L. Kaput and myself. We were particularly interested to observe that two of the communities which we surveyed were in the process of ‘changing over’ from a system of matrilineal inheritance and family residence to a patrilineal one. Data will be presented to show that symptom rates were significantly lower among women who adhered to the old pattern than among those who had changed over. The implications of this finding will be discussed.     

大鼠脑损伤后谷氨酸引起乳酸含量变化的作用机制

目的探讨大鼠脑损伤后谷氨酸引起乳酸含量变化的作用机制。方法28只大鼠随机分为对照组、犬尿烯酸（KYN）灌注组、Ouabain灌注组及Ba^2＋灌注组,每组7只。在建立大鼠局部脑损伤模型前后,应用微透析技术将格林液、KYN、Ouabain和Ba2＋分别灌注到各组大鼠致伤脑区,在致伤前45min开始和致伤后90min内,观察3种药物对脑损伤后乳酸含量的影响。结果对照组伤前乳酸含量为（0.28±0.07）mmol/L,脑损伤后引起乳酸含量迅速升高,伤后15min达到峰值（0.75±0.18）mmol/L,乳酸含量持续升高60min后逐渐下降至接近伤前水平。Ouabain灌注组及KYN灌注组伤后乳酸含量升高幅度减弱,持续时间缩短。Ba^2＋灌注组乳酸含量升高幅度增加,持续时间延长。结论脑损伤后异常增加的谷氨酸作用于兴奋性氨基酸受体偶联离子通道,引起细胞外K^＋增加,使Na^＋-K^＋泵活性增强,继而导致糖酵解代谢水平增高,乳酸含量增加。     

雌激素对去卵巢大鼠缺血再灌注脑损伤的保护作用

目的探讨雌激素对去卵巢大鼠缺血再灌注脑损伤的保护作用。方法将大鼠切除双侧卵巢后30d给予肌肉注射苯甲酸雌二醇100μg/(kg·d)连续14d,然后制作大鼠局灶性脑缺血再灌注模型;制模12h后取脑组织行免疫组化染色,检测细胞间黏附分子(CD54)、肿瘤坏死因子α(TNF-α)的表达;TUNEL法检测脑组织凋亡细胞数;电镜观察脑细胞膜超微结构的变化。结果与缺血再灌注组及去卵巢组比较,雌激素组脑组织CD54、TNF-α表达明显降低,凋亡细胞数明显减少(均P<0.05);脑细胞膜结构非特异性损伤减轻。结论雌激素通过减少缺血再灌注大鼠脑组织炎性细胞因子表达、减轻炎症反应、降低脑组织细胞凋亡而发挥脑保护作用。     

Anti-angiogenic effects of resveratrol on cerebral angiogenesis

Angiogenesis is implicated in diseases of the central nervous system, and its modulation represents an attractive therapeutic strategy. This is the first report of the effects of resveratrol (trans-3,4',5-trihydroxystilbene) on cerebral angiogenesis, using an in vitro model. Processes associated with angiogenesis were studied in cerebral vascular endothelial cells, using the human brain endothelial cell line hCMEC/D3 and primary bovine brain microvessel EC (BBMEC). Comparisons were made to human umbilical vein EC (HUVEC). In cerebral cultures, resveratrol (24h) induced a dose dependent reduction in BrdU incorporation and cell numbers (MTT assay) between 10-100 μM, while lower doses (100 nM-5 μM) had no effect. Cell migration (scratch assay) was inhibited between 10-100 μM depending on cell type. Doses between 10-100 μM reduced average tubule length on Matrigel, while higher doses (50,100 μM) also inhibited process formation around explanted rat aortic rings (ex vivo assay). Cell cycle analysis in hCMEC/D3 (propidium iodide) showed reduced progression to the G2/M phase, with a maximal effect at 25 μM. Resveratrol did not induce apoptosis in hCMEC/D3, based on caspase-3 activity. Cytotoxicity (LDH release) was induced by resveratrol (50,100 μM) in hCMEC/D3 and HUVEC, peaking at ~20% in hCMEC/D3 and ~35% in HUVEC. Cytotoxic effects were not detected in BBMEC. Resveratrol (10-50 μM) inhibited phosphorylation of the serine/threonine kinase Akt, by Western blot (15 min, 1h) with a prolonged inhibition (24h) for 25 μM. In conclusion, this study shows inhibitory effects of resveratrol on cerebral angiogenesis, using an in vitro model. This is discussed in terms of dosage, in vivo equivalence and therapeutic potential.     

Protective effects of acupuncture on brain tissue following ischemia/reperfusion injury★

BACKGROUND： In patients with cerebrovascular disease, by means of the neuroendocrine system, acupuncture supports the transformation of a local pathological status into a physiological status. Recently, great progress has been made in studying the protective effects of acupuncture on brain ischemia/reperfusion injury. OBJECTIVE： To summarize research advances in the protective effects of acupuncture on brain ischemia/reperfusion injury. RETRIEVAL STRATEGY： Using the terms ＂acupuncture, transcutaneous electrical acupoint stimulation, cerebral ischemia/reperfusion injury, and cerebral protection＂, we retrieved articles from the PubMed database published between January 1991 and June 1994. Meanwhile, we searched the China National Knowledge Infrastructure with the same terms. Altogether, 114 articles and their results were analyzed. Inclusive criteria： studies that were closely related to the protective effects of acupuncture on brain ischemia/reperfusion injury, or studies, whose contents were in the same study field and were published recently, or in the authorized journals. Exclusive criteria： repetitive studies. LITERATURE EVALUATION： Thirty articles that related to the protective effects of acupuncture on brain ischemia/reperfusion injury were included. Among them, 7 were clinical studies, and the remaining 23 articles were animal experimental studies. DATA SYNTHESIS： ① Animal experimental studies have demonstrated that acupuncture improves brain blood perfusion and brain electrical activity, influences pathomorphological and ultramicrostructural changes in ischemic brain tissue, is beneficial in maintaining the stability of intracellular and extracellular ions, resists free radical injury and lipid peroxidation, and influences cytokine, neurotransmitter, brain cell signal transduction, and apoptosis-regulating genes. ② Clinical studies have demonstrated that acupuncture not only promotes nutritional supply to local brain tissue in patients with cerebral infarction, but also increases brai