The renin-angiotensin system (RAS) serves as a key regulator of body fluid balance and cardiovascular homeostasis, whose dysregulation is involved in the pathogenesis of various central nervous system (CNS) diseases. Beyond their canonical functions such as vascular regulation, the constituents of the RAS, particularly angiotensin (Ang) II, exert inflammatory and oxidative injury on neurons in the brain. Meanwhile, the non-classical pathway angiotensin-converting enzyme (ACE)2/Ang-(1-7) axis shows beneficial effects against CNS diseases. Activation of cerebral ACE2/Ang-(1-7) exerts regulatory effects on neurons, endothelial cells, glial cells, and other kinds, thereby comprehensively optimizing the blood-brain barrier (BBB), neurovascular unit, and cerebral microenvironment, and ultimately modulating memory, cognition, and emotion. This review, through comprehensive literature retrieval from PubMed and Web of Science, focuses on elucidating the critical regulatory role of the ACE2/Ang-(1-7) axis in CNS diseases and provides an in-depth exploration of its associated physiological and pathological mechanisms. Future research directions will primarily concentrate on novel drug development strategies targeting the ACE2/Ang-(1-7) axis, aiming to optimize drug development potential from multiple perspectives-including BBB penetration, targeted delivery to specific lesion sites, and regulation of pathological microenvironments and targets-to achieve early intervention, precision medicine, and efficient treatment for long-term CNS diseases.

BACKGROUND:Annexin A1 (ANXA1) can be activated by ischemia/reperfusion (I/R) events or inflammatory processes, but its specific regulatory mechanisms need further investigation. METHODS:ANXA1 in BV-2 cells was knocked down or overexpressed, and OGD/R induced injury, while 740YP and LY294002 were used for intervention. Microglia polarization phenotype and marker levels were assessed through flow cytometry, RT-qPCR and western blot. Autophagic flux and lysosomal function were evaluated by mCherry-GFP-LC3B, acridine orange (AO) staining and LysoTracker staining. ANXA1 and PI3K/Akt/mTOR proteins were detected by western blot. The tMCAO/R mouse model was established. Longa score, behavioral test and pathological staining to assess the extent of nerve injury, and microglia polarization and autophagy indicators were detected. RESULTS:ANXA1 expression was decreased in OGD/R-treated microglia. ANXA1 overexpression facilitated the transformation of microglia phenotype from M1-like phenotype to M2-like phenotype, increased CD206 and IL-10 expression, reduced the GFP/mCherry ratio and LysoTracker positive cells, and increased the red fluorescence of AO staining. ANXA1 overexpression also significantly reduced PI3K, Akt and mTOR phosphorylation. Moreover, ANXA1 overexpression markedly decreased Longa score, brain water content and infarct size, improved motor and neurological impairment in tMCAO/R mice, elevated Nissl bodies and Iba-1+CD206+ positive area, and reduced necrotic neuron numbers, inflammatory factor content and autophagy protein levels. In addition, 740YP significantly inhibited the improvement of ANXA1 overexpression, and LY294002 significantly enhanced the improvement of ANXA1 overexpression. CONCLUSION:Overexpression of ANXA1 regulated microglia polarization and autophagic flux via regulating PI3K/Akt/mTOR pathway, and improved cerebral I/R inflammatory injury.

BACKGROUND:Neuronal pyroptosis is involved in neuronal cell death and neurological damage after cerebral ischemia-reperfusion. 14,15-Epoxyeicosatrienoic acid (14,15-EET) can reduce neuronal loss induced by cerebral ischemia-reperfusion by regulating mitochondrial biological processes. However, it remains unclear how 14,15-EET regulates mitochondrial homeostasis, inhibits neuronal pyroptosis, and promotes neurological functional recovery after cerebral ischemia-reperfusion. METHODS:Mice with middle cerebral artery occlusion and reperfusion were used as an animal model to study the cerebral ischemia-reperfusion disease. The neurological function of mice was performed at 1, 3, and 5 days to test the therapeutic effects of 14,15-EET. Transmission electron microscope imaging and Nissl staining were used to analyze neuronal morphological structure, mitophagy, and neuronal pyroptosis. Western blot and transcriptome were used to detect the levels of mitophagy and neuronal pyroptosis signaling pathway-related molecules. HT22 cells were used in in vitro studies to detect the mechanism by which 14,15-EET reduces neuronal pyroptosis after oxygen-glucose deprivation/reoxygenation treatment. RESULTS:14,15-EET treatment reduced cerebral infarct volumes and improved neurological functional recovery in mice after cerebral ischemia-reperfusion. 14,15-EET treatment maintained the morphological structure of neurons in the ischemic penumbra area as well as the dendritic spine density in mice after cerebral ischemia-reperfusion. The upregulation of NLRP1 (NOD-like receptor thermal protein domain associated protein 1), IL (interleukin)-1β, caspase-1, and GSDMD (gasdermin D) induced by cerebral ischemia-reperfusion was inhibited, and the expression of mitophagy proteins Parkin and LC3B (microtubule-associated protein 1 light chain 3 B) was increased by 14,15-EET treatment. Transcriptome profiling found that 14,15-EET exerts a neuroprotection role in promoting neural function recovery by activating the WNT (wingless-type mouse mammary tumor virus integration site family) signaling pathway. We found that 14,15-EET upregulated the WNT pathway proteins such as WNT1, WNT3A, β-catenin, and p-GSK-3β (phosphorylation of glycogen synthase kinase 3β) in vivo and in vitro. The WNT signaling pathway inhibitor XAV-939 reduced the expression of mitophagy protein Parkin and upregulated the expression of caspase-1 and GSDMD in HT22 cells with oxygen-glucose deprivation/reoxygenation and 14,15-EET treatment. CONCLUSIONS:14,15-EET regulates mitochondrial homeostasis to inhibit neuronal pyroptosis, thereby promoting the recovery of neurological function in mice after cerebral ischemia-reperfusion. These results provide new ideas for maintaining mitochondrial homeostasis and inhibiting neuronal pyroptosis after cerebral ischemia-reperfusion.

The p110β isoform of the PI3 kinase (PI3K) family plays a key role in tumorigenesis and PTEN loss-driven multidrug resistance (MDR). Herein, we describe the design, synthesis, and structure-activity relationship studies of a series of small-molecule PI3K/110β PROTACs degraders by combining the selective inhibitor TGX221 of PI3K/110β with VHL ligands. Among them, J-6 and J-9 exhibited rapid and efficient degradation ability for the target proteins in MDR cells. Meanwhile, the expression and activity of P-glycoprotein were significantly inhibited, leading to a strong synergistic antitumor effect with adriamycin or cisplatin. Further studies confirmed that the two degraders can induce endoplasmic reticulum stress-mediated mitochondrial apoptosis by the AKT/Bcl-2 inhibition-mediated PERK/CHOP-unfolded protein reaction. In vivo studies also verified that the two degraders inhibited the growth of MCF-7/ADM xenograft tumors with high safety. Hence, this study and further optimization of these PI3K/110β PROTAC degraders have broad prospects for the development of new cancer therapies.

This study aims to explore the neuroprotective effect of bilobalide(BB) and the mechanisms such as inhibiting inflammatory response in macrophage/microglia, promoting neurotrophic factor secretion, and interfering with the activation and differentiation of peripheral CD4~+ T cells. BB of different concentration(12.5, 25, 50, 100 μg·mL~(-1)) was used to treat the RAW264.7 and BV2 cells for 24 h. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay and cell counting kit-8(CCK-8) were employed to detect the cytotoxicity of BB and appropriate concentration was selected for further experiment. Lipopolysaccharide(LPS) was applied to elicit inflammation in RAW264.7 and BV2 cells, mouse bone marrow-derived macrophages(BMDMs), and primary microglia, respectively. The effect of BB on cell proliferation and secretion of inflammatory cytokines and neurotrophic factors was detected by enzyme-linked immunosorbent assay(ELISA). Spleen monocytes of C57BL/6 female mice(7-8 weeks old) were isolated, and CD4~+ T cells were separated by magnetic beads under sterile conditions. Th17 cells were induced by CD3/CD28 and the conditioned medium for eliciting the inflammation in BMDMs. The content of IL-17 cytokines in the supernatant was detected by ELISA to determine the effect on the activation and differentiation of CD4~+ T cells. In addition, PC12 cells were incubated with the conditioned medium for eliciting inflammation in BMDMs and primary microglia and the count and morphology of cells were observed. The cytoto-xicity was determined by lactate dehydrogenase(LDH) assay. The result showed that BB with the concentration of 12.5-100 μg·mL~(-1) had no toxicity to RAW264.7 and BV2 cells, and had no significant effect on the activity of cell model with low inflammation. The 50 μg·mL~(-1) BB was selected for further experiment, and the results indicated that BB inhibited LPS-induced secretion of inflammatory cytokines. The experiment on CD4~+ T cells showed that the conditioned medium for LPS-induced inflammation in BMDMs promoted the activation and differentiation of CD4~+ T cells, while the conditioned medium of the experimental group with BB intervention reduced the activation and differentiation of CD4~+ T cells. In addition, BB also enhanced the release of neurotrophic factors from BMDMs and primary microglia. The conditioned medium after BB intervention can significantly reduce the death of PC12 neurons, inhibit neuronal damage, and protect neurons. To sum up, BB plays a neuroprotective role by inhibiting macrophage and microglia-mediated inflammatory response and promoting neurotrophic factors.

目的 研究精细化护理联合天智颗粒在遗忘型轻度认知功能障碍(aMCI)患者管理中的应用效果.方法 选取 aMCI患者 120 例,按随机数表法分为研究组和对照组,每组 60 例.对照组采用常规护理联合天智颗粒治疗,研究组采取精细化护理联合天智颗粒治疗.比较 2 组认知功能[蒙特利尔认知评估量表(MoCA)评分]、安全隐患事件发生情况及护理满意度.结果 干预后 2 组 MoCA 总分均较干预前升高,且研究组高于对照组(均 P＜0.001);研究组护理满意度高于对照组(88.4%比 75.0%,P＜0.01).住院护理期间,研究组和对照组总安全隐患事件发生率分别为 6.7%和 8.3%,2 组比较差异无统计学意义(P＞0.05).结论 精细化护理联合天智颗粒在 aMCI患者管理中具有积极的效果,可提升患者的认知功能和护理满意度.

目的 研究姜黄素类似物Cur20对乙酰胆碱酯酶(AChE)的作用,评价其对阿尔茨海默病(AD)的治疗潜力.方法 昆明小鼠随机分4组:对照组、模型组、姜黄素(20 μmol·kg-1)组和Cur20(20 μmol·kg-1)组,每天ig给药1次,给药体积10mL·kg-1,除对照组外,其他各组小鼠每次给药30min后ip东莨菪碱1mg·kg-1制备AD模型,共给药16d.第11天开始进行5 d的Morris水迷宫实验,第16天进行Y迷宫实验,检测小鼠的行为认知情况;第17天处死小鼠,取脑分离出海马组织,试剂盒法检测乙酰胆碱(ACh)含量;体外实验检测姜黄素和Cur20对AChE、丁酰胆碱酯酶(BuChE)活性的影响;分子对接实验预测Cur20与AChE的作用模式.结果 小鼠实验结果表明,与模型组比较,Cur20在总游泳距离、游泳速度无显著差异的情况下,能够显著降低水迷宫的逃避潜伏期、增加目标象限的停留时间和路程比例(P＜0.05、0.01),明显增加平台穿越次数;在入臂次数无显著性差异的情况下,Cur20组小鼠的自发交替率明显升高;Cur20组海马组织ACh水平显著升高(P＜0.01).体外实验结果表明,Cur20对AChE的半数抑制浓度(IC50)为(32.44±4.46)μmol·L-1,50μmol·L-1 Cur20对BuChE抑制率为(-1.8±2.3)％,Cur20对AChE的抑制作用具有良好的选择性.分子对接实验表明Cur20能与AChE的活性部位结合.结论 Cur20能抑制AChE活性、提高ACh含量,显著改善东莨菪碱所致的学习记忆损伤,可能是一种潜在的治疗AD的药物.

目的 探讨帕金森病(PD)患者危险因素.方法 选取本院2015年1月至2018年12月PD患者90例作为PD组,另按照1:1的比例选取同期同科室就诊的其他疾病患者90例作为非PD组,分析影响PD发生的危险因素.结果 在婚状态、存在饮酒史人群PD发生率与其他人群比较差异无统计学意义(P>0.05);农民、杀虫剂接触史人群PD发生率高于其他职业人群,受教育程度较高、进行规律的体育锻炼、参与户外娱乐活动、饮茶、经常进行阅读和写作人群PD发生率低于其他人群,差异有统计学意义(P<0.05);Logisitic回归分析显示职业、杀虫剂接触史是PD发生的独立危险因素,受教育程度高、规律的体育锻炼、积极参与户外娱乐活动、饮茶、经常进行阅读与写作是PD发生的保护因素.结论 筛查PD发生的相关影响因素对于开展PD的预防具有一定程度的指导意义,有利于延缓PD发生进展.

目的:探讨规范化教学查房在神经病学规范化培训中的应用及效果.方法:选取2018年6月至2020年12月在神经内科轮转的住院医师规范化培训人员200例作为研究对象,随机分为规范化教学查房组(100人)和传统教学查房组(100人).分析两组人员轮转结束后的考核成绩(病例书写、体格检查、临床思维、理论考核等)和问卷调查教学评价(自主学习能力、临床问题处理等的提升)的差异.结果:规范化教学查房组考核项目中的病例书写、体格检查、技能操作、临床思维、疾病掌握、医患沟通、治疗方案、护理评价及整体表现得分均高于传统教学查房组(P<0.05),两组的理论考核成绩无明显差异(P>0.05).问卷调查教学评价结果显示:规范化教学查房组人员的临床问题处理能力、临床技能操作能力及临床思维能力的提升程度明显高于传统教学查房组(P<0.05),两组自主学习能力的提升无明显差异(P>0.05).结论:规范化教学查房在神经病学规范化培训中可明显提升规培人员的临床业务能力,值得在神经病学规范化培训中推广应用.

目的 观察盐酸美金刚联合益智醒脑汤治疗帕金森痴呆的临床疗效.方法 将2019年1月—2020年3月焦作市第二人民医院收治的72例帕金森痴呆病人作为研究对象,采用随机数表法分为单药组(采用盐酸美金刚治疗)与联合组(采用盐酸美金刚+益智醒脑汤治疗),各36例,两组均治疗16周.比较两组临床疗效、中医证候积分、认知功能[蒙特利尔认知评估量表(MoCA)、简易智能精神状态检查量表(MMSE)]、血清炎症指标[白细胞介素-1β(IL-1β)、白细胞介素-17(IL-17)、同型半胱氨酸(Hcy)、肿瘤坏死因子-α(TNF-α)]和氧化指标[超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化酶(GSH-Px)]及不良反应.结果 联合组总有效率高于单药组,差异均有统计学意义(86.11％与63.89％,P<0.05).治疗后,两组中医证候积分和血清IL-1β、IL-17、Hcy、TNF-α、MDA水平较治疗前均下降,MoCA、MMSE评分和SOD、GSH-Px水平均升高,且联合组优于单药组,差异有统计学意义(P<0.05).联合组不良反应发生率低于单药组,但差异无统计学意义(11.11％和16.67％,P>0.05).结论 盐酸美金刚联合益智醒脑汤治疗帕金森痴呆安全有效,可抑制炎症,减轻氧化应激反应,改善病人认知功能.

Subarachnoid hemorrhage (SAH) is one of the common clinical neurological emergencies. Its incidence accounts for about 5–9% of cerebral stroke patients. Even surviving patients often suffer from severe adverse prognoses such as hemiplegia, aphasia, cognitive dysfunction and even death. Inflammatory response plays an important role during early nerve injury in SAH. Toll-like receptors (TLRs), pattern recognition receptors, are important components of the body’s innate immune system, and they are usually activated by damage-associated molecular pattern molecules. Studies have shown that with TLR 4 as an essential member of the TLRs family, the inflammatory transduction pathway mediated by it plays a vital role in brain injury after SAH. After SAH occurrence, large amounts of blood enter the subarachnoid space. This can produce massive damage-associated molecular pattern molecules that bind to TLR4, which activates inflammatory response and causes early brain injury, thus resulting in serious adverse prognoses. In this paper, the process in research on TLR4-mediated inflammatory response mechanism in brain injury after SAH was reviewed to provide a new thought for clinical treatment.

Insomnia can cause damage to function and other medical and mental illnesses, and it is also a risk factor for increasing medical care costs. Although simple behavior intervention is feasible in primary medical institutions, the lack of corresponding technical training has obviously restricted its use, patients' autonomy dependence is generally poor, and early missions have some difficulties. Relatively speaking, acupuncture in traditional therapy is more likely to be accepted, but the mechanism is still unclear. In this study, a model of insomnia was constructed using chlorophenylalanine (PCPA) in 6-week-old male SD rats. Electroacupuncture was used to stimulate Baihui (DU20), Shenmen (HT7), and Sanyinjiao (SP6), and the behavior, histopathology, cAMP/CREB/BDNF, PI3K/Akt pathways and the expression of sleep-related factors were observed. Our study showed that IL-1β, PGD2, MT, IL-10, IL-6, TNF-α, IFN-γ and CORT in rats could be regulated after electroacupuncture stimulation. The expression of TrkB, PI3K, Akt, P-TrkB, p-Akt, cAMP, CREB, and BDNF can also be up- or downregulated. Apoptosis-related Bax, Bad and Caspase-3, as well as the monoamine neurotransmitters 5-HT, DA, NE and EPI, were also modulated by electroacupuncture. Taken together, these data illustrate the potential of DU20, HT7 and SP6 as a multitargeted therapy for insomnia in rats. The novelty of the study lies in the description of the Traditional Chinese Medicine stimulation methods different from Chinese Herbs: electroacupuncture stimulates acupoints of sleep factors, cAMP/CREB/BDNF, PI3K/Akt pathways and the multipath and multitarget body response regulation mechanism of apoptosis.

免疫炎症反应在脑血管疾病的病理生理机制中发挥着重要作用.最新的研究表明,全身免疫炎症指数(SⅡ)作为一种新型的炎症标志物,综合多种炎性细胞,可以更全面地反映局部免疫和全身炎症反应的平衡状态,并与多种脑血管病(如脑梗死、脑出血、静脉窦血栓形成、颅内动脉瘤等)的发生、发展及临床预后相关,因其潜在的临床应用价值,越来越受临床工作者的关注.本文对近年来SII在脑血管疾病中的研究进展进行阐述.

目的:探讨磁敏感加权成像(SWI)与磁共振弥散张量成像(DTI)在帕金森病综合征中的诊断价值.方法:选取本院2017年9月-2020年4月收治的原发性单侧症状帕金森病综合征患者70例作为帕金森组(n=70),同期选择健康体检者70例作为对照组(n=70).两组均进行SWI和DTI检查,收集两组感兴趣区(红核、壳核、苍白球、黑质和丘脑)的表观弥散系数(ADC值)、各项异性分数(FA值)及校正相位数(CP值)之间的差异,并采用受试者工作特征曲线(ROC)分析感兴趣区相关参数对单侧症状帕金森病综合征的预测效能.结果:帕金森组症状同侧和症状对侧感兴趣区ADC值与对照组比较差异无统计学意义(P>0.05);帕金森组症状同侧和症状对侧红核、壳核、苍白球及丘脑的FA值、CP值与对照组比较差异无统计学意义(P>0.05);帕金森组症状对侧黑质FA值低于症状同侧(P<0.05),症状对侧黑质CP值高于症状同侧(P<0.05);症状对侧黑质FA值的灵敏度为72.68％,特异度为81.06％,准确度为78.31％,曲线下面积为0.722(0.581～0.854);症状对侧黑质CP值的灵敏度为80.06％,特异度为88.72％,准确度为83.15％,曲线下面积为0.837(0.720～0.913).结论:原发性单侧症状帕金森病综合征患者的症状对侧黑质FA值及CP值均较高,其对该疾病的早期诊断具有一定价值.

Objective:To analyze the effect of rivastigmine combined with selegiline on patients with Parkinson disease (PD) and its influence on serum β-amyloid protein 1-42 (Aβ1-42), and insulin-like growth factor-1 (IGF-1) levels.Methods:A total of 102 patients with PD admitted to First Affiliated Hospital of Henan University from May 2019 to July 2020 were selected, and they were divided into observation group and control group by random number table method, with 51 patients in each group. The patients in the control group were given oral administration of selegiline; based on the treatment of control group, patients in the observation group were given oral administration of rivastigmine. All patients received 3 months of treatment. The clinical effects, unified Parkinson disease rating scale (UPDRS) scores, scales for outcomes in Parkinson disease-autonomic questionnaire (SCOPT-AUT) scores, montreal cognitive assessment (MoCA) scores, Berg balance scale (BBS) scores, serum Aβ1-42, IGF-1 levels before and after treatment, and adverse reactions were compared between the two groups.Results:The effective rate of the observation group was 90.20% (46/51), higher than the 70.59% (36/51) of the control group ( P<0.05). After treatment, the UPDRS scores and SCOPT-AUT scores of the observation group were lower than those of the control group, while the MoCA scores and BBS scores were higher than those of the control group ( P<0.05). After treatment, serum levels of Aβ1-42 and IGF-1 in the observation group were higher than those in the control group ( P<0.05). There was no significant difference in the incidence of adverse reactions between observation group (19.61%, 10/51) and control group (14.75%, 9/51), P<0.05. Conclusions:The combination of rivastigmine and selegiline is effective in the treatment of patients with PD. It can reduce the UPDRS scores and autonomic symptoms, and improve cognitive function, balance ability, serum Aβ1-42 and IGF-1 levels, with good safety.

目的 研究分析脑血流灌注情况对遗忘型轻度认知功能障碍(aMCI)患者认知功能的影响因素.方法 选取2018年1月至2020年1月本院收治的aMCI 186例神经内科就诊患者,其中aMCI患者86例作为a MCI组,门诊非神经系统疾病患者100例作为正常组,采用简易智能表(MMSE)及韦氏记忆量表(WMS)对2组患者的认知功能进行评价;采用西门子Symbia T2型单子发射计算机断层测定血流灌注量.结果 aMCI组患者MMSE、短时记忆量表、长时记忆量表及瞬时记忆量表得分小于正常组(P<0.05);aMCI组患者在右侧额叶、双侧颞叶、双侧顶叶及右侧枕叶等部位血流灌注量明显小于正常组(P<0.05);aMCI组患者MMSE评分与其呈正相关的部位脑结构有右侧额叶、左侧顶叶及双侧颞叶等部位脑血流量(P<0.05),其他部位脑结构脑血流量与MMSE评分无相关性(P>0.05).结论 额叶、颞叶、枕叶、顶叶等部位脑区血流灌注参数与认知功能障碍有着一定的联系.

帕金森病的冻结事件严重降低患者的生活质量，增加致残率。可穿戴设备的兴起在帕金森病等慢性病领域开拓了广泛的应用前景。本文对可穿戴设备在帕金森病冻结步态领域的应用进行综述，为探讨冻结步态可能的运动学机制，量化冻结步态评估，完善冻结步态的管理提供有力的依据。

〔目的〕观察阿尔茨海默病患者血清ICAM-1、VCAM-1和Aβ-42水平的变化及脂必泰胶囊的作用.〔方法〕 随机挑选了96例阿尔茨海默病患者,并将其分为对照组(n=48)和观察组(n=48).两组阿尔茨海默病患者均使用多奈呱齐片5 mg,1次/d,常规口服治疗.在此基础上,观察组增加了脂必泰胶囊0.24 g,2次/d,口服治疗12周.比较两组患者治疗前后血清中ICAM-1水平、VCAM-1水平、MoCA评分和Aβ-42水平的变化.〔结果〕观察组血清中ICAM-1、VCAM-1和Aβ-42水平低于治疗前和同期对照组,差异有统计学意义(P<0.05);观察组MoCA评分治疗后明显高于治疗前(P<0.05),而对照组治疗前后MoCA评分差异无统计学意义(P>0.05).〔结论〕 脂必泰胶囊可能通过降低阿尔茨海默病患者血清ICAM-1、VCAM-1水平,减少Aβ-42的生成,提高其认知功能.

目的 探讨产后抑郁患者给予超觉静坐法联合心理治疗干预后其睡眠质量及情绪变化.方法 选取我院85例产后抑郁患者,应用掷币法分为心理组42例及超觉组43例,心理组患者采用常规心理疏导进行治疗,超觉组患者加用超觉静坐治疗,对比两组患者治疗后抑情绪、睡眠质量、生活质量、婴儿照护能力及临床疗效.结果 超觉组总有效率、婴儿照护能力及SF-36评分高于心理组(P＜0.05),ERDS、PSQI评分低于心理组(P＜0.05).结论 超觉静坐技术联合心理治疗能够有效提升产后抑郁患者的婴儿照护能力,改善其情绪及睡眠质量,提升患者的生活质量.

Neuroinflammation is considered as an important mechanism of vascular dementia (VaD). Our primary study showed that the bisindole analogue (2-(2-(bis(5-chloro-1H-indol-3-yl)methyl)phenoxy)aniline, compound 4ae) had great anti-inflammation in zebrafish. Rat model of permanent occlusion of the bilateral common carotid arteries (2-vessel occlusion, 2VO) was utilized to evaluate the neuroprotective effect of 4ae. Our results showed that 4ae treatment effectively reduced Iba-1 positive microglia cells in cerebral cortex and hippocampus after cerebral ischemia. Compared with the model group, neuroinflammation characterized by Interleukin (IL)-6 and tumor necrosis factor (TNF)-α, oxidative stress characterized by reactive oxygen species (ROS) and superoxide dismutase (SOD) were both improved significantly after treatment with 4ae. Moreover, 4ae treatment significantly reversed ischemia-induced ACE enhancement, while notably increased the level of ACE2. To further elucidate the role of 4ae on neuroinflammation, we investigated the effects of 4ae on lipopolysaccharide (LPS)-induced inflammation in BV2 microglia cells, a kind of innate immune cells in central nervous system. The results demonstrated that the expressions of CD11b, TNFα and IL-6 and the level of ROS were up-regulated after treatment with LPS. More importantly, 4ae was able to block the activation of BV2 by reducing ROS production and the expression of inflammatory cytokines. In addition, our results suggested that 4ae inhibited the inflammatory response mediated by microglia cells by inhibiting NF-κB. This anti-inflammatory effect on microglia may be a potential mechanism for the neuroprotective effect of 4ae in VaD.