目的:探讨经颅直流电刺激(tDCS)联合盐酸舍曲林对老年抑郁症患者的疗效及对认知功能和血清脑源性神经营养因子(BDNF)水平的影响.方法:62例老年抑郁症患者随机分为tDCS组和伪tDCS组;两组在舍曲林治疗基础上分别给予真、伪tDCS治疗4周.分别于治疗前及治疗后1、2、4周末进行汉密尔顿抑郁量表(HAMD)、治疗中出现的症状量表(TESS)评估;治疗前后采用数字广度测验(DST)及威斯康星卡片分类测试(WCST)评估认知功能;治疗前后测定两组血清BDNF水平.结果:治疗前两组各项评估及检查结果比较差异无统计学意义.治疗后,两组HAMD评分均明显低于治疗前,且tDCS组明显低于伪tDCS组(P均<0.05);两组认知功能均较治疗前明显改善,其中tDCS组DST中的正序评分及总分明显高于伪tDCS组;两组血清BDNF水平均较前明显升高且tDCS组明显高于伪tDCS组(P均<0.05);两组不良反应发生率差异无统计学意义.结论:盐酸舍曲林联合tDCS治疗老年抑郁症疗效以及认知功能改善更优,可能与联合治疗提高了血清BDNF水平有关.

Sevoflurane preconditioning (SPC) results in cerebral ischemic tolerance; however, the mechanism remains unclear. Promoting microglia/macrophages polarization from pro-inflammatory state to anti-inflammatory phenotype has been indicated as a potential treatment target against ischemic stroke. In this study, we aimed to assess the effect of SPC on microglia polarization after stroke and which signaling pathway was involved in this transition.Mouse primary microglia with SPC were challenged by oxygen-glucose deprivation (OGD) or lipopolysaccharide (LPS), and mice with SPC were subjected to middle cerebral artery occlusion (MCAO). Then, the mRNA and protein levels of pro-inflammatory/anti-inflammatory factors were analyzed. GSK-3β phosphorylation and Nrf2 nuclear translocation were measured. The mRNA and protein expression of pro-inflammatory/anti-inflammatory factors, neurological scores, infarct volume, cellular apoptosis, the proportion of pro-inflammatory/anti-inflammatory microglia/macrophages, and the generation of super-oxidants were examined after SPC or GSK-3β inhibitor TDZD treatment with or without Nrf2 deficiency.Sevoflurane preconditioning promoted anti-inflammatory and inhibited pro-inflammatory microglia/macrophages phenotype both in vitro and in vivo. GSK-3β phosphorylation at Ser9 was increased after SPC. Both SPC and TDZD administration enhanced Nrf2 nuclear translocation, reduced pro-inflammatory microglia/macrophages markers expression, promoted anti-inflammatory markers level, and elicited a neuroprotective effect. Nrf2 deficiency abolished the promoted anti-inflammatory microglia/macrophages polarization and ischemic tolerance induced by TDZD treatment. The reduced percentage of pro-inflammatory positive cells and super-oxidants generation induced by SFC or TDZD was also reversed by Nrf2 knockdown.Our results indicated that SPC exerts brain ischemic tolerance and promotes anti-inflammatory microglia/macrophages polarization by GSK-3β-dependent Nrf2 activation, which provides a novel mechanism for SPC-induced neuroprotection.

Electroacupuncture (EA) pretreatment induces cerebral ischemic tolerance; however, the mechanism remains poorly understood. This study aimed to determine the participation of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-mediated mitochondrial biogenesis in the neuroprotection of EA and whether cannabinoid receptor 1 (CB1R) is involved in this mechanism. At 2 hours after EA pretreatment, adult male C57BL/6j mice were subjected to 60-minute right middle cerebral artery occlusion (MCAO). Mitochondrial function, the level of mitochondrial biogenesis-related proteins (nuclear transcription factor 1, NRF1; mitochondrial transcription factor A, TFAM), and mitochondrial DNA (mtDNA) were measured. A small interfering RNA (siRNA) targeting PGC-1α and the CB1R antagonists AM251 and SR141716A were given to the animals before EA pretreatment, and mitochondrial function and biogenesis were examined after MCAO. EA ameliorated the mitochondrial function, upregulated the NRF1 and TFAM expression, and increased the mtDNA levels and the volume and number of mitochondria. EA pretreatment increased the expression of PGC-1α, whereas the PGC-1α siRNA and CB1R antagonists reversed the improved neuroprotection and increased mitochondrial biogenesis induced by EA. Our results indicated that EA pretreatment protects the mitochondria and promotes mitochondrial biogenesis by activating CB1R-dependent PGC-1α, which provides a novel mechanism for EA pretreatment-induced ischemic tolerance.

The current study was designed to seek the role of the glycogen synthase kinase-3β (GSK-β)-regulated NF-E2-related factor 2 (Nrf2) pathway in the antioxidant effect induced by Apigenin-7-O-β-D-(-6”-p-coumaroyl)-glucopyranoside (APG). Rat primary cultured cortical neurons were challenged by oxygen and glucose deprivation/reoxygenation (OGD/R) and then treated with APG. Cell viability, phosphorylation of GSK-β at Ser9 and nuclear expression of Nrf2 were measured. Male Sprague Dawley rats challenged by 2-h middle cerebral artery occlusion were treated with 50 mg/kg APG, and the neurological score, infarct volume, phosphorylation of GSK-3β and nuclear expression of Nrf2 were analyzed. The neuroprotective effect of APG and the expression levels of antioxidant enzymes and oxidative products were also examined in the presence and absence of Nrf2-siRNA and PI3K inhibitors. APG reduced the apoptotic proportion, attenuated LDH release and increased cell viability, and in vivo, APG improved neurological scores and reduced infarct volume. APG increased GSK-3β phosphorylation and Nrf2 nuclear translocation, while these effects were prevented by PI3K inhibitors or Nrf2-siRNA treatment in both OGD/R cell cultures and ischemic/reperfusion rats. These findings reveal that GSK-3β phosphorylation-mediated Nrf2 activation is involved in the neuroprotective effect of APG.

Repetitive transcranial magnetic stimulation (rTMS) treatment is widely accepted as an evidence-based treatment option for depression and anxiety. However, the underlying mechanism of this treatment maneuver has not been clearly understood. The chronic unpredictable mild stress (CUMS) procedure was used to establish depression and anxiety-like behavior in rats. The rTMS was performed with a commercially available stimulator for seven consecutive days, and then depression and anxiety-like behaviors were subsequently measured. The expression of nuclear factor-E2-related factor 2 (Nrf2) was measured by western-blot, and the level of tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), and interleukin-6 (IL-6) was measured with Enzyme-linked immunesorbent assay (ELISA) analyzing kits. Furthermore, a small interfering RNA was employed to knockdown Nrf2, after which the neurobehavioral assessment, Nrf2 nuclear expression, and the amount of inflammation factors were evaluated. Application of rTMS exhibited a significant antidepressant and anxiolytic-like effect, which was associated with the increased Nrf2 nuclear translocation and reduced level of TNF-α, iNOS, IL-1β, and IL-6 in the hippocampus. Following Nrf2 silencing, the antidepressant and anxiolytic-like effect produced by rTMS was abolished. Moreover, the elevated Nrf2 nuclear translocation, and the reduced production of TNF-α, iNOS, IL-1β, and IL-6 in hippocampus mediated by rTMS, were reversed by Nrf2 knockdown. Together, these results reveal that the Nrf2-induced anti-inflammation effect is crucial in regulating antidepressant-related behaviors produced by rTMS.

Abstract Background: Sevoflurane preconditioning (SPC) results in cerebral ischemic tolerance; however, the mechanism remains unclear. In current study, we aimed to assess the M1/M2 shift in the brain induced by SPC and whether glycogen synthesis kinase-3β (GSK-3β)-regulated nuclear factor erythroid 2-related factor (Nrf2) activation was involved in the M2 polarization mediated by SPC. Methods: Mouse primary microglia with SPC were challenged by oxygen-glucose deprivation (OGD) or lipopolysaccharide (LPS), and mice with SPC were subjected to middle cerebral artery occlusion (MCAO). Then, the mRNA and protein levels of proinflammatory/anti-inflammatory factors were analysed. GSK-3β phosphorylation and Nrf2 nuclear translocation were measured. The mRNA and protein expression of proinflammatory/anti-inflammatory factors, neurological scores, infarct volume, cellular apoptosis, the proportion of M1/M2-positive cells, and the generation of super-oxidants were examined after SPC or GSK-3β inhibitor TDZD treatment with or without Nrf2 deficiency. Results: SPC promoted M2 phenotype polarization both in vitro and in vivo . GSK-3β phosphorylation at Ser9 was increased after SPC. Both SPC and TDZD administration enhanced Nrf2 nuclear translocation, promoted M2 phenotype polarization and elicited a neuroprotective effect. Nrf2 deficiency abolished the promoted M2 polarization and ischemic tolerance induced by TDZD treatment. The reduced percentage of M1-positive cells and super-oxidants generation induced by SFC or TDZD was also reversed by Nrf2 knockdown. Conclusions: Our results indicated that SPC exerts brain ischemic tolerance and enhances M2 polarization by GSK-3β-dependent Nrf2 activation, which provides a novel mechanism for SPC-induced neuroprotection.

创伤后应激障碍(PTSD)发病受多种因素影响,生物学机制是PTSD发病机制的重要组成,对深入理解PTSD、寻找客观的诊断标志物以及研发新型PTSD治疗药物十分重要.脑影像、光遗传及化学遗传学技术等神经科学研究技术的进展揭示了脑结构、脑功能以及神经环路改变在PTSD发病中的重要作用.但由于PTSD临床表现复杂、症状组合不同,目前未有一致性结论.因此,本综述尝试根据PTSD诊断的症状分类,从临床影像与基础环路研究两个方面归纳、总结PTSD不同症状的神经环路异常机制,从而为阐明PTSD发病机制、寻找客观生物标志物、筛选全新治疗靶点提供新的思路.

创伤后应激障碍（PTSD）发病受多种因素影响，生物学机制是PTSD发病机制的重要组成，对深入理解PTSD、寻找客观的诊断标志物以及研发新型PTSD治疗药物十分重要。脑影像、光遗传及化学遗传学技术等神经科学研究技术的进展揭示了脑结构、脑功能以及神经环路改变在PTSD发病中的重要作用。但由于PTSD临床表现复杂、症状组合不同，目前未有一致性结论。因此，本综述尝试根据PTSD诊断的症状分类，从临床影像与基础环路研究两个方面归纳、总结PTSD不同症状的神经环路异常机制，从而为阐明PTSD发病机制、寻找客观生物标志物、筛选全新治疗靶点提供新的思路。

It is known that preconditional treatment with volatile anesthetics can induce tolerance of the brain to stroke. A previous study demonstrated that the involvement of TREK-1, a two-pore domain K+ channel, in sevoflurane preconditioning induced neuroprotection against focal cerebral ischemia in rats. The present study testified whether TREK-2, another anesthetic-target K+ channel, is also associated with volatile anesthetic-induced neuroprotection, and further explored its potential mechanism. Rats preconditioned with isoflurane were subjected to 1.4vol% isoflurane plus 98% O-2 (1.5 L/min) inhalation for 1 hour daily and continuing for 5 consecutive days. Then, these rats were subjected to middle cerebral artery occlusion (MCAO) as focal cerebral ischemia model. The expression of TWIK-related K+ channel 2 (TREK-2) was analyzed by western blotting and quantitative real-time RT-PCR, and its downstream signaling molecules, protein kinase C (PKC) alpha, extracellular signal-regulated kinase 1/2 (ERK1/2), and pERK1/2 were detected by western blotting also. Subsequently, the expression of TREK-2 was regulated by siRNA transfection in the brain to clarify its role in the neuroprotection of isoflurane preconditioning. Neurological scores, infarction volume, and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining were examined to evaluate the outcomes. The impact of TREK-2 on the expression of its downstream signaling molecules was also examined for preliminary analysis of the possible mechanisms. Isoflurane preconditioning reduced the infarct volume, inhibited the cell apoptosis, and improved the neurological outcome in rats subjected to MCAO. These effects were parallel with the increase in TREK-2 protein and inhibition of the ERK1/2 phosphorylation. The downregulation of TREK-2 through siRNA could significantly attenuate the isoflurane preconditioning-induced neuroprotective effects. Isoflurane preconditioning-induced neuroprotective effects against ischemia-reperfusion injury are associated with the increase in TREK-2 channel activation. These effects depend on the attenuation of PKC alpha and inhibition of ERK1/2 phosphorylation. Results enrich our understanding on the mechanism of two-pore domain K+ channel in preconditioning-induced tolerance to focal cerebral ischemia.

Tanshinone IIA (TSA), a principal component derived from the Traditional Chinese Medicine Danshen has been suggested to exert neuroprotective effect against experimental cerebral ischemic/reperfusion injury. But the associated underlying mechanisms still have not been understood. The current study characterized the role of nuclear factor erythroid two-related factor-induced antioxidant response in the neuroprotective efficacy of TSA treatment. The focal cerebral ischemia/reperfusion model was established by 60-minute middle cerebral artery occlusion. At the onset during reperfusion, mice were treated with 10 mg/kg TSA intraperitoneally. The mRNA and nuclear factor erythroid 2 (Nrf2) protein expression, the antioxidant enzymes, and oxidative production levels were measured. To further verify the role of Nrf2 in the neuroprotective effect induced by TSA, the Nrf2 small silenced RNA and Nrf2 knockout mice were used, the neurological function, brain infarct volume, and cellular apoptosis examination were assessed. TSA treatment improved neurological scores, reduced infarct volume, and attenuated the cellular apoptosis. TSA treatment upregulated the expression of Nrf2 mRNA and the contents of Nrf2 protein in nuclear extract. Nrf2 activation by TSA treatment increased the contents of antioxidant enzymes, and reduced the generation of oxidative productions. Either Nrf2 knockdown or Nrf2 knockout abolished the antioxidative and neuroprotective effect of TSA treatment. These results demonstrate that the Nrf2 activation contributes to TSA-induced neuroprotection from experimental ischemic stroke through maintaining antioxidant effect.

Background: Microglia can not only detrimentally augment secondary injury but also potentially promote recovery. However, the mechanism underlying the regulation of microglial phenotypes after stroke remains unclear. Methods: Mice were subjected to middle cerebral artery occlusion for 60 min. At 3 days after reperfusion, the effects of activation and suppression of triggering receptor expressed on myeloid cells 2 on immunocyte phenotypes (n = 5), neurobehavioral scores (n = 7), infarct volumes (n = 8), and neuronal apoptosis (n = 7) were analyzed. In vitro, cultured microglia were exposed to oxygen–glucose deprivation for 4 h. Inflammatory cytokines, cellular viability (n = 8), neuronal apoptosis (n = 7), and triggering receptor expressed on myeloid cells 2 expression (n = 5) were evaluated in the presence or absence of triggering receptor expressed on myeloid cell-specific small interfering RNA or triggering receptor expressed on myeloid cells 2 overexpression lentivirus. Results: Triggering receptor expressed on myeloid cells 2 expression in the ischemic penumbra peaked at 3 days after ischemia–reperfusion injury (4.4 ± 0.1-fold, P = 0.0004) and was enhanced in interleukin-4/interleukin-13–treated microglia in vitro (1.7 ± 0.2-fold, P = 0.0119). After oxygen–glucose deprivation, triggering receptor expressed on myeloid cells 2 conferred neuroprotection by regulating the phenotypic conversion of microglia and inflammatory cytokine release. Intraperitoneal administration of triggering receptor expressed on myeloid cells 2 agonist heat shock protein 60 or unilateral delivery of a recombinant triggering receptor expressed on myeloid cells 2 lentivirus into the cerebral ventricle induced a significant neuroprotective effect in mice (apoptotic neurons decreased to 31.3 ± 7.6%; infarct volume decreased to 44.9 ± 5.3%). All values are presented as the mean ± SD. Conclusions: Activation or up-regulation of triggering receptor expressed on myeloid cells 2 promoted the phenotypic conversion of microglia and decreased the number of apoptotic neurons. Our study suggests that triggering receptor expressed on myeloid cells 2 is a novel regulator of microglial phenotypes and may be a potential therapeutic target for stroke.

Background: Stroke is a severe disease and the associated molecular mechanisms for its pathogenesis have not been fully understood. Myocyte enhancer factor 2 (MEF2) is a family of transcription factors that promote the expression of more than 100 proteins responsible for development and surviving of neurons in central nervous system. Recently, it is reported in animal studies that MEF2D dysfunction plays an important role in neurodegenerative diseases. However, the role of MEF2D in stroke is unknown. The objective of the present study was to provide data for changes and role of MEF2 following hypoxic neuronal injury. Methods: The hypoxic injury was induced by oxygen-glucose deprivation (OGD) in primary cultured rat cortical neurons. The levels and activity of MEF2D mRNA and protein were measured by real-time reverse transcription polymerase chain reaction (RT-PCR) and western blot. Additionally, MEF2D overexpression by lentivirus was used to up-regulate the level of MEF2D. The effect of MEF2D up-regulation on neuron hypoxic tolerance was evaluated by assaying of cell viability and extracellular lactate dehydrogenase (LDH) release as well as cell apoptosis analysis.Results: Compared with control group, the level of MEF2D protein and the activity of MEF2D were decreased after OGD challenge. Up-regulating the level of MEF2D could increase the cell viability, decrease the LDH release and inhibit the activation of apoptotic protein caspase-3.Conclusion: MEF2D is involved in the pathophysiological process of hypoxic injury in rat primary cortical neurons. Up-regulation of MEF2D could alleviate the hypoxia-induced injury and increase neuronal tolerance against hypoxia. Citation: Li-Kai Shi, Min Cai, Zhi-Xin Wu, Si-Si Sun, Zong-Ping Fang, Ting Gu, et al. Up-regulating MEF2D alleviates hypoxia-induced injury in cultured rat cortical neurons. J Anesth Perioper Med 2015; 2: 175-82. doi: 10.24015/JAPM.2015.0024This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

We investigated whether glutamate receptor subunit 2 (GluR2) is involved in EA pretreatment-induced neuroprotection via cannabinoid CB1 receptors (CB1R) after global cerebral ischemia in mice. Two hours after electric acupuncture (EA) pretreatment, global cerebral ischemia (GCI) was induced by bilateral common carotid artery occlusion (BCCAO) for 20 min. The GluR2 expression was examined in the hippocampus after reperfusion. Cell survival, neuronal apoptosis, the Bax/Bcl-2 ratio and neurological scores were evaluated at 24 h after BCCAO in the presence or absence of the GluR2 inhibitor. Furthermore, the GluR2 was determined in the presence and absence of CB1R inhibitor. Our results showed EA pretreatment enhanced expression of GluR2 in the hippocampus 2 h after reperfusion. Moreover, EA pretreatment improved neurological outcome, promoted cell survival, inhibited neuronal apoptosis, and decreased the Bax/Bcl-2 ratio after reperfusion. GluR2 knockdown by GluR2 siRNA effectively reversed the beneficial effects of EA pretreatment. Furthermore, CB1R siRNA and two CB1R antagonists blocked the elevation of GluR2 expression by EA pretreatment, whereas the two CB1R agonists up-regulated GluR2 expression as EA pretreatment. In conclusion, GluR2 up-regulation is involved in neuroprotection of EA pretreatment against GCI through CB1R, suggesting that GluR2 may be a novel target for stroke intervention.

Electroacupuncture (EA) pretreatment elicits the neuroprotective effect against cerebral ischemic injury through cannabinoid receptor type 1 receptor (CB1R). In current study, we aimed to investigate whether the signal transducer and activator of transcription 3 (STAT3) and manganese superoxide dismutase (Mn-SOD) were involved in the antioxidant effect of EA pretreatment through CB1R. At 2 h after EA pretreatment, focal cerebral ischemic injury was induced by transient middle cerebral artery occlusion for 60 min in C57BL/6 mice. The expression of Mn-SOD in the penumbra was assessed by Western blot and immunoflourescent staining at 2 h after reperfusion. In the presence or absence of Mn-SOD small interfering RNA (siRNA), the neurological deficit score, the infarct volume, the terminal deoxynucleotidyl transferase-mediated dUDP-biotin nick end labeling (TUNEL) staining, and oxidative stress were evaluated. Furthermore, the Mn-SOD protein expression and phosphorylation of STAT3 at Y705 were also determined in the presence and absence of CB1R antagonists (AM251, SR141716) and CB1R agonists (arachidonyl-2-chloroethylamide (ACEA), WIN 55,212-2). EA pretreatment upregulated the Mn-SOD protein expression and Mn-SOD-positive neuronal cells at 2 h after reperfusion. EA pretreatment also attenuated oxidative stress, inhibited cellular apoptosis, and induced neuroprotection against ischemic damage, whereas these beneficial effects of EA pretreatment were reversed by knockdown of Mn-SOD. Mn-SOD upregulation and STAT3 phosphorylation by EA pretreatment were abolished by two CB1R antagonists, while pretreatment with two CB1R agonists increased the expression of Mn-SOD and phosphorylation level of STAT3. Mn-SOD upregulation by EA attenuates ischemic oxidative damage through CB1R-mediated STAT3 phosphorylation in stroke mice, which may represent one new mechanism of EA pretreatment-induced neuroprotection against cerebral ischemia.

Background Adiponectin,an adipokine secreted by different adipocytes,has been known to play pivotal roles in metabolisms including insulin sensitization,oxidation of glucose and lipids.Recently,it has been reported that adiponectin can also attenuate the process of atherosclerosis,decrease the inflammatory response,protect myocardia against ischemic reperfusion injury,and provide neuroprotection.Objective To review the related clinical studies of adiponection as a factor to assess the risk and the prognosis of ischemic stroke and basic studies about the mechanism of exogenous adiponectin induced neuroprotection against ischemic stroke injury.Content In present review,we described the recent advances in the relationship between serum adiponectin and occurrence of ischemic stroke in clinic trials and the mechanism of neuroprotection induced by supplement of adiponectin.Trend Mounting clinical studies indicate that low level of serum adiponectin is associated with high incidence and poor outcomc of ischemic stroke.Furthermore,some basic researches also demonstrate the neuroprotective effects of exogenous adipokine.

内源性大麻素系统包括大麻素受体、内源性配体以及参与其合成与降解的酶类,在人体内广泛分布,参与诸多生理和病理生理过程.新近报道内源性大麻素系统在中枢神经系统的许多疾病的病理生理过程中扮演重要的角色.对内源性大麻素系统的研究,不仅能阐明一些疾病的病理生理机制,还有助于新药研发并为疾病治疗提供新的方向.本文基于现有的文献报道,就内源性大麻素系统及其在一些中枢神经疾病特别是脑缺血和帕金森病的发病机制的新进展进行综述.

目的:探讨Peroxiredoxin 6(Prx6)在电针预处理诱导的SD大鼠脑缺血耐受中的作用.方法:健康雄性SD大鼠80只,随机分为4组:假手术组(Sham组,n＝16)、单纯电针组(Electro acupuncture组,EA组,n＝16)、局灶性脑缺血再灌注组[通过大脑中动脉栓塞制作脑缺血再灌注(middle cerebral artery occlusion,MCAO)模型,MCAO组,n＝32],其中2、6、12、24、48 h各4只和电针预处理组(EA+ MCAO组,n＝ 16).通过梗死容积及神经功能评分(Garcia评分)评价脑损伤程度;通过Western Blot检测Prx 6在脑缺血再灌注后的表达水平;通过Western Blot和免疫组织化学染色法检测电针预处理对Prx 6表达的影响.结果:与MCAO组相比,EA+ MCAO组梗死容积减少,神经功能评分显著改善(P＜0.05);与Sham组相比,Prx 6在MCAO模型后再灌注24h时表达最高(P＜0.05);与Sham组相比,再灌注后24h时MCAO组Prx 6表达水平升高(P＜0.05);与MCAO组相比,再灌注后24 h时EA+ MCAO组Prx 6的表达水平进一步升高(P＜0.05).结论:电针预处理通过促进缺血再灌注后Prx 6的表达升高而发挥脑保护作用.

Objective The effect of electroacupuncture( EA) pretreatment on the expression of manganese superoxide dismutase( SOD2) after cerebral ischemia and reperfusion is investigated.Methods Adult male C57mice were randomly divided into 4 groups: sham,EA,middle cerebral artery occlusion( MCAO),EA + MCAO. Cerebral ischemic injury was induced by transient middle cerebral artery occlusion( tMCAO) at 2 h after EA pretreatment.The expression of SOD2was analyzed by Western blot and immuneflourescence staining at 2 h after reperfusion. At24 h after reperfusion,the infarction volume and neurological scores were evaluated and the apoptotic cells were examined by transferase-mediated deoxyuridine triphosphate-biotin nick end labeling( TUNEL) staining. Results At2 h after reperfusion,the expression of SOD2in MCAO group was decreased,and EA pretreatment increased the content of SOD2at 2 h after reperfusion compared with MCAO group. EA pretreatment improved the neurological behaviors and attenuated the infarct volume in EA + MCAO group. EA pretreatment reduced the number of apoptotic cells in penumbra. Conclusion EA pretreatment increases the expression of SOD2,which may be involved in the neuroprotection induced by EA pretreatment.

目的:观察高血容量血液稀释(hypervolemic hemodilution,HHD)对老年患者围术期血流动力学的影响.方法:选取20名无心脏病史的麻醉手术患者;10名患者＞ 65周岁,10名＜55周岁.所有人试患者在术前接受相同的HHD处理(60 g/L羟乙基淀粉静脉输注,15 ml/kg).在血液稀释后不同时间使用经食管多普勒超声监测(transesophageal Doppler monitoring,TDM)患者的血流动力学变化,同时监测患者血细胞比容(Hct)、血红蛋白、血气及心电变化.结果:所有患者手术期间均未发生任何并发症.两组患者间的一般资料、生化检查数据、Hct、血气等均无统计学差异.HHD后对照组(＜55周岁)的心排出量(cardiac output,CO)升高,老年组(＞65周岁)降低.对照组的心率(heart rate,HR)下降和心搏指数(stroke index,SI)升高(P＜0.05),而老年组HR无明显改变,SI轻微下降.血液稀释后对照组患者的外周血管阻力值有明显下降(P＜0.05),而老年患者出现了升高的趋势.结论:无心脏病史的老年患者并不能很好耐受术前急性高容量血液稀释.HHD可以导致由SI下降所致的CO下降.