Galectins-8 (Gal-8), the tandem repeat sequences of the galectin family, can influence the pathophysiologic processes in neurological disorders. However, its effect on intracerebral hemorrhage and related mechanisms remains nebulous. Using collagenase VII-S-induced ICH in the left striatum of mice, we investigated the effects of Gal-8 on cellular and molecular immune inflammatory responses in hemorrhagic brain and evaluated the severity of short- and long-term brain injury. Our results showed that activated microglia in the periphery of hematoma in mice with intracerebral hemorrhage expressed Gal-8, while Gal-8 could regulate the expression of cytokines, such as HMGB-1 (P = 0.0032), TNF-α (P = 0.0158), and IL-10 (P =0.0379). Inhibition of the glucose-binding activity of Gal-8 by thiogalactoside (TDG) significantly reduced the volume of cerebral hematoma (P = 0.0241) and hydrocephalus (P = 0.0112) during the acute phase of cerebral hemorrhage and improved the long-term prognosis. TDG can reduce acute-phase brain tissue injury and improve the prognosis by inhibiting the activation of immune-inflammatory cells in the periphery of hematoma and reducing the release of pro-inflammatory factors.

Ischemic preconditioning (IPC) is an approach of protection against cerebral ischemia by inducing endogenous cytoprotective machinery. However, few studies in neurogenesis and oligodendrogenesis after IPC have been reported, especially the latter. The purpose of this study is to test our hypothesis that IPC may also induce cell proliferation and oligodendrogenesis in the subventricular zone and striatum, as well as to investigate the effect of nuclear factor erythroid 2-related factor 2 (Nrf2) on oligodendrogenesis. IPC was induced in mice by 12-min ischemia through the occlusion of the middle cerebral artery. Newly generated cells were labeled with 5-bromo-2′-deoxyuridine. Our findings demonstrated that IPC stimulated the proliferation of neural stem cells in the subventricular zone, promoted the generation of oligodendrocyte precursor cells in the striatum and corpus callosum/external capsule (CC/EC), and stimulated oligodendrocyte precursor cells differentiation into oligodendrocytes in the striatum and the CC/EC. Furthermore, we describe a crucial role for Nrf2 in IPC-induced oligodendrogenesis in the subventricular zone, striatum, and CC/EC and show for the first time that Nrf2 promoted the migration and differentiation of oligodendrocyte precursor cells into oligodendrocytes in the striatum and CC/EC. Our data imply that IPC stimulates the oligodendrogenesis in the brain and that Nrf2 signaling may contribute to the oligodendrogenesis.

Alzheimer’s disease (AD) is the most common neurodegenerative disease and is manifested by memory loss and spatialdisorientation. There is currently no effective treatment for AD. Abnormalities of the chromosome 9 open reading frame72 (C9orf72) gene have been associated with various neurodegenerative diseases. However, its intrinsic roles in AD remainto be elucidated. Here we found that Aβ25‑35 increased the expression of C9orf72 in PC12 cells at both mRNA and proteinlevels. In Aβ25‑35‑treated PC12 cells, C9orf72 overexpression induced an abnormally condensed and fragmented nucleus andapoptosis, as well as significantly enhanced reactive oxygen species (ROS) levels. Mechanistically, an Aβ25‑35‑induced decreaseof superoxide dismutase activity was augmented by C9orf72 overexpression, which in contrast increased malondialdehydecontent. Consistently, further apoptotic analysis revealed significant downregulation of Bcl‑2 and Bcl‑xL expression andenhanced cleavage of caspase‑3 with Aβ25‑35 treatment, all of which were exacerbated by C9orf72 overexpression. In addition,tau phosphorylation, another hallmark of AD pathology, was induced by Aβ25‑35 and was remarkably enhanced by C9orf72overexpression. Our data indicate that C9orf72 plays important roles in intracellular ROS signaling and Aβ25‑35‑induced neuronalapoptosis in AD. These findings provide insights into C9orf72 function in the pathogenesis of many related neurodegenerativediseases and provide a basis for potential therapeutic interventions.

目的 基于磷酯酰激醇3-激酶/蛋白激酶B/一氧化氮合酶(PI3K/Akt/NOS)通路探讨鞣花酸对脑缺血再灌注损伤大鼠的神经保护作用.方法 将36只雄性Wistar大鼠按数字表法随机分为3组:假手术(Sham)组、缺血再灌注组和鞣花酸预干预组,线栓法制作大鼠右侧大脑中动脉缺血120 min再灌注模型.鞣花酸预干预为造模前14 d按100 mg/(kg·d)给予鞣花酸灌胃,每组12只.运用神经功能缺损评分法评估各组动物的行为学变化,H E染色观察各组大鼠缺血侧脑组织病理改变,Western blotting法检测缺血侧脑组织凋亡蛋白及PI3K/Akt/NOS信号通路蛋白.结果 (1)鞣花酸可以提高缺血再灌注后神经功能评分(P<0.05).(2)模型组大鼠缺血侧脑组织凋亡相关蛋白(Bax/Bcl-2、CytC、Cleaved caspase-3)水平比Sham组明显升高(P<0.05),鞣花酸组大鼠缺血侧脑组织凋亡相关蛋白(Bax/Bcl-2、CytC、Cleaved caspase-3)水平比模型组组明显减少(P<0.05).(3)模型组大鼠缺血侧脑组织中(p-Akt/Akt及p-eNOS/eNOS)比Sham组明显降低(P<0.05),鞣花酸组大鼠缺血侧脑组织中(p-Akt/Akt及p-eNOS/eNOS)明显升高(P<0.05).结论 鞣花酸可以激活PI3K/Akt通路减轻大鼠脑缺血再灌注损伤,保护脑组织.

目的 探讨盐酸多奈哌齐联合高压氧治疗血管性认知障碍临床疗效.方法 将存在血管性认知障碍的90例患者随机分为治疗组(n=47例)和对照组(n=43例),对照组给予多奈哌齐及脑血管病基础治疗,治疗组在对照组基础上联合高压氧物理治疗,观察治疗前后MMSE及MoCA评分变化.结果 治疗前存在不同程度认知障碍,但MMSE及MoCA评分比较差异无统计学意义,治疗后2组认知功能均改善,MMSE及MoCA评分均提高,与对照组比较治疗组评分显著提高,2组比较差异有统计学意义(P＜0.05).结论 血管性认知障碍患者在常规血管病及多奈哌齐治疗基础上联合高压氧物理治疗,能显著改善患者认知障碍,且无明特殊不良反应,安全有效,实用范围广.

目的 探讨影响卒中后抑郁(PSD)患者院外抗抑郁药物服用依从性的影响因素.方法 收集251例PSD患者的年龄、性别、教育水平、婚姻状况、居住地、既往史、脑卒中亚型、NIHSS评分(评价神经功能受损的严重程度)、PHQ-9量表评分(评价患者抑郁症状的严重程度)、住院天数及服用的抗抑郁药物(艾司西酞普兰、氟西汀、黛力新、阿米替林等)等信息.随访出院后6个月时以调查问卷的形式了解患者的主要照顾人、抗抑郁药物的服用天数、服用效果(服用抗抑郁药物后抑郁症状对比服药前有无明显好转)、药物价格承担能力(患者或其主要照顾人对药物价格的主观感受),以及有无出现影响停止服药的不良反应.将服用抗抑郁药物天数≥总随访天数的50％纳入依从性好组,<50％纳入依从性差组.比较两组上述收集指标,并对有统计学意义的指标进行二元逐步Logistic回归分析.结果 出院后6个月,依从性好组96例(38.25％),依从性差组155例(61.75％).两组性别、教育水平、居住地、药物价格、药物服用效果、主要照顾人、酗酒史、住院和出院NIHSS评分、出院PHQ-9评分、住院天数比较差异有统计学意义(P<0.05或<0.01).Logistic回归分析结果显示,抗抑郁药物良好依从性与PHQ-9评分高(P<0.01,OR=1.475,95％CI=1.306～1.666)、药物效果自觉良好(P=0.013,OR=2.348,95％CI=1.194～4.616)、有家人陪伴(P=0.006,OR=0.147,95％CI=0.038～0.573)相关.结论 PSD患者院外抗抑郁药物服用依从性受多方面因素影响,PHQ-9量表评分高、抗抑郁药物自觉效果良好、有家人陪伴均能提高患者的抗抑郁药物服用依从性.

目的:探讨Solitaire-AB型支架于颅内基底动脉闭塞取栓手术中的应用效果及其安全性.方法:选取郑州大学附属洛阳中心医院神经介入科使用Solitaire-AB型支架进行基底动脉取栓术治疗的20例急性脑梗死患者,并对其临床资料进行回顾性分析,记录、比较术内即时取栓疗效及术后6个月的随访结果.结果:闭塞血管成功获得再通有19例,未见手术相关并发症.13例患者在术后24 h内临床症状得到明显好转,1周后下床活动,在出院后随访3个月内症状基本消退;1例患者术后24h神经系统功能未见明显恢复,经随访6个月可生活自理;2例患者治疗效果欠佳,随访6个月仍然遗留严重的神经系统后遗症;1例血管未开通患者于术后第3天因脑疝死亡.术后随访6个月16例患者的MRS评分为1～2分,即达到术后再通良好的效果.结论:Solitaire-AB型支架在颅内基底动脉闭塞取栓手术中的应用可有效提高闭塞血管再通率,显著改善基底动脉闭塞的预后.

Characterization of the rupture risk factors for small intracranial aneurysms (SIAs, ≤5 mm) is clinically valuable. The present study aims to identify image-based morphological parameters and anatomical locations associated with the rupture status of SIAs. Two hundred and sixty-three patients with single SIAs (128 ruptured, 135 unruptured) were included, and six morphological parameters, including size, aspect ratio (AR), size ratio (SR), height–width ratio (H/W), flow angle (FA) and aneurysm width–parent artery diameter ratio, and the aneurysm locations were evaluated using three-dimensional geometry, and were used to identify a correlation with aneurysm rupture. Statistically significant differences were observed between ruptured and unruptured groups for AR, SR, H/W, FA, and aneurysm locations, from univariate analyses. Logistic regression analysis further revealed that AR (p = 0.034), SR (p = 0.004), H/W (p = 0.003), and FA (p < 0.001) had the strongest independent correlation with ruptured SIAs after adjustment for age, gender and other clinical risk factors. A future study on a larger SIA cohort need to establish to what extent the AR, SR, H/W and FA increase the risk of rupture in patients with unruptured SIAs in terms of absolute risks.

Background: Transtemporal Doppler (TTD) with middle cerebral artery (MCA) is widely used for right-to-left shunt (RLS) detection. However, an alternative method for patients without suitable temporal bone windows should be established. The present study prospectively evaluated the effectiveness of transorbital Doppler (TOD) with carotid siphon (CS) monitoring in detecting RLS. Methods: A total of 357 subjects with sufficient temporal bone windows underwent simultaneous TTD with MCA and TOD with CS. After injection of microbubbles, the numbers of artificial high-intensity signals were recorded at rest and after Valsalva maneuver. Results: TOD with CS detected RLS in 146 patients. Sensitivity was 97.1%, specificity 95%, positive predictive value 92.5%, and negative predictive value 98.1%. The total positive rates for RLS detection by CS (40.9%) and MCA (37.8%) monitoring were comparable without significant difference, but TOD with CS detected significantly more grade 2 and 3 RLS than TTD with MCA (p = 0.001). The RLS rates of cryptogenic stroke patients was significantly higher than that of healthy controls, and RLS in cryptogenic stroke was remarkably higher than that in transient ischemia attack patients (p < 0.05). TOD with CS examined significantly more grade 2 and 3 RLSs than the MCA approach in the cryptogenic stroke patients (p = 0.037). Conclusion: TOD with CS monitoring is able to detect RLS effectively in different populations including healthy subjects, cryptogenic stroke, transient ischemia attack, and migraine patients. In comparing to the TTD with MCA approach, TOD with CS monitoring could detect comparable rate of RLS, but more high grades of RLS.

Ischemic stroke is the leading cause of worldwide mortality and long-term disability in adults. This study aims to explore the effects of RNA interference (RNAi)-mediated silencing of the S100B gene on nerve function recovery and morphological changes of hippocampus cells in rat models with ischemic stroke. Sixty Wistar rats were assigned into different group. S100B and Caspase 3 mRNA and protein expressions were evaluated by RT-qPCR and Western blotting. Positive rate of S100B, NeuN, and MAP2 expressions were detected by immunohistochemistry (IHC). Water content, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activity in brain tissues were measured. Enzyme-linked immunosorbent assay (ELISA) was employed to detect serum levels of TNF-α and IL-1β. A neurological severity score (NSS) was used to test nerve function. TUNEL assay was used to determine hippocampal cell apoptosis. Downregulation of S100B showed a lower number of S100B immune positive cells, but higher NeuN and MAP2-positive cells, increased SOD level, declined MDA level, prominently faster recovery of neurological function, decreased TRCS, TCTP, TCFP, and IE levels, an obvious increase in the number of survival neurons, a decrease in the number of apoptotic cells, notably decreased TNF-α and IL-1β contents, as well as infarct volume, an obvious decrease in positive hippocampal cell Caspase 3 expression and protein expressions of Caspase 3 and cleaved Caspase 3. This study provides data to suggest that RNAi-mediated silencing of S100B gene could improve the recovery of nerve function while inhibiting apoptosis of hippocampal cells in rats with ischemic stroke.

Microglial over-activation and apoptosis are associated with ischemic brain diseases. These processes may be hindered by oxysophocarpine (OSC) that generates anti-inflammatory and anti-apoptotic activities. However, the precise roles of OSC in microglial inflammation and apoptosis induced by oxygen-glucose deprivation/reoxygenation (OGD/R) remain unclear. In this study, we found that OSC reduced OGD/R-induced inflammation in BV-2 microglia. OSC elevated cell viability and prevented the release of lactate dehydrogenase. OSC downregulated cyclooxygenase 2 and inducible nitric oxide synthase and reduced the levels of inflammatory mediators, including tumor necrosis factor-α, interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1, prostaglandin E2, and nitric oxide. OSC inhibited the expression of Toll-like receptor 4 (TLR4) and myeloid differentiation protein 88 (MyD88) and blocked the activation of nuclear factor (NF)-κB. In addition, OSC suppressed OGD/R-elicited BV-2 cell apoptosis, as indicated as follows: The restored mitochondrial membrane potential and the reduced caspase-3 activity; the decrease of Bax and cleaved caspase-3 and the increase of Bcl-2; the enhanced phosphorylation of Akt and mTOR. These results implied that OSC impedes OGD/R-induced inflammation and apoptosis of microglial cells. Therefore, OSC may be potentially used for ischemic stroke therapy.

The protective potential of ethyl pyruvate (EP) on neuron has been investigated previously. This study was intended to investigate the effects of EP on the severity of oxygen-glucose deprivation (OGD)-induced injury in neural-like PC12 cells. PC12 cells were exposed to OGD condition with or without EP treatment. Then, cell viability, apoptosis, and the expressions of neurotrophic factors were detected. Further, Sprague-Dawley rats were intravenously administered with 5mg/kg EP for 14 days post-middle cerebral artery occlusion (MCAO). The effects of EP on the infarct volumes and neurological functions of MCAO rats were then assessed. Result showed that EP alleviated OGD-diminished cells viability, OGD-induced apoptosis, and OGD-reduced expressions of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and Nestin in PC-12 cells. EP blocked OGD-activated the Notch1 and nuclear factor Kappa B (NF-κB) signaling pathways in PC12 cells. Besides, in vivo data demonstrated that EP treatment decreased infarct volume and mNSS score, and increased the time spent on the rota-rod apparatus of MCAO rats. To conclude, EP protected neural-like PC12 cells from cerebral ischemia-reperfusion injury by suppressing apoptosis and promoting neural restoration. Notch1 and NF-κB pathway might implicated in the functions of EP on neuron.

Strokes are a major cause of disability and death worldwide. An association between microRNA-146a (miR-146a) and miR-149 polymorphisms and strokes was inconclusive. This meta-analysis aimed to reevaluate the strength of the association by searching online databases and retrieving relevant case-control studies published between 2000 and 2016. Nine articles including 8 on miR-146a rs2910164 G/C and 3 on miR-149 rs2292832 C/T in 3372 patients with stroke and 4394 controls were included. The miR-149 rs2292832 was significantly associated with the risk of a stroke under allelic (C vs T: odds ratio [OR] = 1.14; 95% confidence interval [CI] = 1.01-1.29; P = .03), homologous (CC vs TT: OR = 1.36; 95% CI = 1.05-1.77; P = .02), and recessive models (CC vs CT + TT: OR = 1.34; 95% CI = 1.05-1.71; P = .02). No correlation was detected between miR-146a rs2910164 and susceptibility to a stroke. In conclusion, the results suggested that miR-149 might be a risk factor for the development of a stroke, while miR-146a might not be. Well-designed studies with large populations are needed to clarify the association between miR-146a and miR-149 polymorphisms and strokes.

Background: MiR-155 is highly expressed in many malignant tumors with poor prognosis, however its role in glioma is largely unknown. In this study, we aims at investigating the clinical significance of miR-155, and further exploring the targeted regulation of F-box and WD repeat domain containing 7 (FBXW7) mRNA. Material/Methods: Forty-five serum samples, 66 tissues and paired adjacent noncancerous tissues from primary glioma patients were collected and used to detect the expression of miR-155 and FBXW7 mRNA by RT-qPCR. Protein expression of glioma cells were detected by western blot and the cell proliferation and apoptosis was also evaluated. Results: The expression of miR-155 was significantly increased in both serum and primary tissues from primary glioma patients, and enhanced miR-155 level was associated with tumor size, WHO grade and Karnofsky Performance Status (KPS). The Cox regression multivariate analysis showed that miR-155 was an independent prognostic factor of over survival for glioma patients. The gain and loss-function experiments revealed that miR-155 promoted cell proliferation and inhibited apoptosis. Furthermore, FBXW7 was identified as the direct target of miR-155. FBXW7 is a tumor suppressor gene through directly suppressing glioma cell growth and promoting apoptosis. Moreover, FBXW7 significantly abrogated the miR-155-induced cell proliferation and apoptosis effects. Conclusions: High level of miR-155 expression was correlated with enhanced malignant potential and poor prognosis of glioma patients. Furthermore, miR155 could promote cell proliferation and suppress apoptosis through directly suppressing FBXW7 expression. Thus, miR-155 may be a novel prognostic biomarker and therapeutic target in glioma patients.

Epigallocatechin-3-gallate (EGCG) is the major effective component of green tea and has been known as a potential anticancer drug because of its antioxidant and anti-angiogenic properties. EGCG has also been reported to have preventive effects against ischemic stroke via nuclear factor erythroid 2-related factor 2 (Nfr2) signaling pathway, but how EGCG affect angiogenesis after stroke remains unclear. In this study, we investigated whether EGCG treatment in the acute phase of ischemic stroke can promote angiogenesis in a mouse model of transient middle cerebral artery occlusion (MCAO). We assessed neurological function with modified neurologic severity score (mNSS) test, infarct volume by Nessl staining, angiogenesis and oxidative stress by immunofluorescence analysis, intravital lectin perfusion analysis, western blot analysis and enzyme-linked immunosorbent assay (ELISA). In order to explore the role of Nrf2 in the angiogenesis of MCAO + EGCG-treated mice, we used MAPK/ERK inhibitor PD98059 to block the activation of Nrf2. We found MCAO + EGCG-treated mice had better neurologic outcome, less infarct volume, more number of Ki67/CD31-positive vessels, higher vascular density, unregulated VEGF-VEGFR2 signaling pathway, increased Nrf2 expression and decreased oxidative stress than did MCAO + vehicle-treated mice. Blocking Nrf2 with PD98059 significantly reduced the expression of Nrf2, increased oxidative stress and abolished the angiogenic and neuroprotective effects of EGCG on MCAO mice. We conclude that EGCG treatment in the early stage of ischemic stroke can promote angiogenesis in MCAO mice, possibly via upregulation of Nrf2 signaling pathway.

This study aimed to identify the key differentially expressed genes (DEGs) following ischemic stroke (IS).The GSE22255 microarray dataset, which contains samples from peripheral blood mononuclear cells of 20 IS patients and 20 sexand age-matched controls, was downloaded from the Gene Expression Omnibus. After data pre-processing, DEGs were identified using the Linear Models for Microarray Data package in R. The Search Tool for the Retrieval of Interacting Genes database was used to predict the interactions among the products of DEGs, and then Cytoscape software was used to visualize the protein-protein interaction (PPI) network. DEGs in the PPI network were then analyzed using the Database for Annotation, Visualization, and Integrated Discovery online software to predict their underlying functions through functional and pathway enrichment analyses.A total of 144 DEGs were identified in IS samples compared with control samples, including 75 upregulated and 69 downregulated genes. Genes with higher degrees in the PPI network included FOS (degree=26), TP53 (degree=22), JUN (degree=20), EGR1 (degree=18), JUNB (degree=16), and ATF3 (degree=15), and these genes may function in IS by interacting with each other (e.g., EGR1-JUN, EGR1-TP53, ATF3-FOS, and JUNB-FOS). Functional enrichment analysis indicated that the downregulated TP53 gene was enriched in immune response and protein targeting categories.ATF3 and EGR1 may have an important protective effect on IS, whereas FOS, JUN, and JUNB may be associated with the development of IS. In addition, TP53 may function as an indicator of poor prognosis for IS through its association with the immune response and protein targeting.

1病例资料 患者 女,54岁,以"进行性四肢麻木无力、饮水呛咳3 d"为主诉于2016-08-15入我院神经内科.患者3 d前腹泻后出现全身酸痛,随之四肢麻木,远端为重,伴四肢无力,饮水呛咳、吞咽困难、颈部发硬、气短,至县医院住院治疗,查头颅CT未见明显异常,以"吉兰-巴雷综合征"为诊断,予以营养神经等对症治疗,患者自觉症状进行性加重,遂来我院.行磁共振示双侧延髓内侧急性梗死.既往高血压史8 a,冠心病史5 a,正规治疗.体格检查:T 36.2 ℃,P 82次/min,R 19次/min,Bp 154/96 mmHg,心肺腹无异常.神经系统检查:神志清楚,言语流利,双瞳孔等大等圆,直径约3.0 mm,对光反射灵敏,眼球运动自如,无震颤,余脑神经检查无异常,四肢肌力Ⅳ级,四肢肌张力正常,四肢腱反射(+++),病理征阳性,四肢深感觉减退,浅感觉正常,双侧指鼻试验正常,颈强直.

Caffeic acid is a type of phenolic acid and organic acid. It is found in food (such as tomatoes, carrots, strawberries, blueberries and wheat), beverages (such as wine, tea, coffee and apple juice) as well as Chinese herbal medicines. In the present study, we examined the effects of caffeic acid on learning deficits in a rat model of Alzheimer's disease (AD). The rats were randomly divided into three groups: i) control group, ii) AD model group and iii) caffeic acid group. Caffeic acid significantly rescued learning deficits and increased cognitive function in the rats with AD as demonstrated by the Morris water maze task. Furthermore, caffeic acid administration resulted in a significant decrease in acetylcholinesterase activity and nitrite generation in the rats with AD compared with the AD model group. Furthermore, caffeic acid suppressed oxidative stress, inflammation, nuclear factor‑κB‑p65 protein expression and caspase‑3 activity as well as regulating the protein expression of p53 and phosphorylated (p-)p38 MAPK expression in the rats with AD. These experimental results indicate that the beneficial effects of caffeic acid on learning deficits in a model of AD were due to the suppression of oxidative stress and inflammation through the p38 MAPK signaling pathway.

Objective: This study aimed to explore whether the regulatory effect of miR-21 on alpha-synuclein expression in neurons is a potential mechanism by which geniopside (GP) protects the central nervous system from Parkinson disease (PD).Methods: The human neuroblastoma cell line SH-SY5Y was induced to differentiate in vitro and treated with dimethyl sulfoxide (DMSO), N-methyl-4-phenylpyridinium iodide (MPP+), and MPP+ together with GP. To identify the role of miR-21 in the regulation of lysosome-associated membrane protein 2 (LAMP2A) and alpha-synuclein, SH-SY5Y cells pretreated with MPP+ were transfected with miR-21 mimic and miR-21 inhibitor. To identify whether GP could reduce the level of alpha-synuclein through miR-21/LAMP2A, SHSY5Y cells pretreated with GP were treated with miR-21 mimic or miR-21 inhibitor; meanwhile, a luciferase reporter assay was performed to confirm the direct target of miR-21. LAMP2A was overexpressed using a pCMV6-XL5-LAMP2A vector to confirm the role of LAMP2A in the regulation of alpha-synuclein by miR-21. In these in vitro experiments, the RNA and/or protein expressions of miR-21, LAMP2A, and alpha-synuclein in SH-SY5Y cells were determined by quantitative real-time polymerase chain reaction and/or western blotting, respectively. An in vivo PD mouse model was established through intraperitoneal injection with N-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP). The mice were treated with saline, MPTP, MPTP+GP, and MPTP+GP+miR-21 agomir. The numbers of TH+ cells in the substantia nigra in different groups of mice were compared. The RNA and/or protein expressions of miR-21, LAMP2A, and alpha-synuclein were also determined.Results: The level of miR-21 in the cells or mice models was significantly higher than that in normal cells or normal mice, respectively, and GP significantly downregulated miR-21. GP also raised the protein and mRNA expressions of LAMP2A and reduced the protein level of alpha-synuclein in PD models. MiR-21 upregulated the expression of alpha-synuclein by directly targeting 3' UTR of LAMP2A. LAMP2A overexpression abolished the upregulating effect of miR-21 mimic on alpha-synuclein. MiR-21 mimics/agomir reversed the GP-induced downregulation of alpha-synuclein; miR-21 inhibitor effectively increased the downregulation of alpha-synuclein caused by GP.Conclusion: GP exhibits neuroprotective properties by inhibiting alpha-synuclein expression in PD models through the miR-21/LAMP2A axis. Copyright (C) 2016 Elsevier B.V. All rights reserved.