lncRNA LINC01089对氧糖剥夺/复氧损伤后小胶质细胞极化的影响

目的 探讨长链非编码RNA(lncRNA)LINC01089对小胶质细胞氧糖剥夺/复氧（OGD/R）损伤后表型和炎症反应的影响及其机制。方法 体外培养小鼠小胶质细胞B-V2细胞,OGD/R损伤后,转染lncRNA LINC01089过表达质粒及其空载质粒、沉默质粒siRNA及阴性对照,以及miR-449c-5p模拟物、抑制剂及其阴性对照寡核苷酸。采用qRT-PCR检测M1型小胶质细胞标记物iNOS mRNA和CD86 mRNA、M2型小胶质细胞标记物Arg1 mRNA和CD206 MRNA、lncRNA LINC01089、miR-449c-5p的表达水平;采用ELISA检测细胞上清液炎性因子的含量;采用免疫印迹法检测细胞STAT6蛋白表达水平。荧光素酶报告基因实验验证lncRNA LINC01089与miR-449c-5p以及miR-449c-5p与STAT6的靶向关系。结果 OGD/R损伤后,B-V2细胞lncRNA LINC01089表达水平显著下调,miR-449c-5p表达水平显著上调。荧光素酶报告基因实验结果显示,lncRNA LINC01089靶向负调控miR-449c-...     

miR-127-3p通过下调靶基因MAPK4抑制神经胶质瘤增殖的机制研究

目的 探讨miR-127-3p在神经胶质瘤中的表达水平差异及生物学作用。方法 用RT-PCR法检测神经胶质瘤患者及健康人群脑脊液中miR-127-3p相对表达水平; 用RT-PCR法检测人神经胶质瘤细胞株和人正常神经胶质细胞中的miR-127-3p相对表达水平; 用瞬时转染法上调神经胶质瘤细胞U251中的miR-127-3p相对表达水平,用MTT法检测细胞增殖,用流式细胞术检测细胞凋亡,用Western blot检测凋亡相关蛋白bcl-2、Mcl-1和bax表达水平; Targetscan等在线靶基因预测软件预测miR-127-3p的靶基因,并采用双荧光素酶报告试验和Western blot验证miR-127-3p与靶基因之间的直接作用关系。结果 神经胶质瘤患者(1.33±0.12)脑脊液中的miR-127-3p相对表达水平低于健康人群(3.62±0.26)(t=5.867,P=0.004); U251(0.59±0.05)、U373(0.96±0.08)、U87(0.77±0.03)、SHG44(1.28±0.05)中miR-127-3p相对表达水平均低于人脑正常胶质细胞株HEB(3.64±0.26)(P<0.01); 转染后24、48、72 h 150组、100组和50组细胞吸光度值均低于对照组(P<0.05),并且随着miR-127-3p mimics转染水平增高,U251细胞吸光度值越低; miR-127-3p mimics转染组(39.3±4.6%)细胞早期凋亡率高于对照组(7.2±0.6%)(P<0.05); miR-127-3p mimics转染组(9.3±2.3%)细胞晚期凋亡率高于对照组(2.4±0.5%)(P<0.05); mimic转染组(0.119±0.008)U251细胞bcl-2蛋白表达水平低于对照组(0.556±0.039),mimic转染组(0.168±0.015)U251细胞bax蛋白表达水平高于对照组(0.086±0.006),mimic转染组(0.144±0.009)U251细胞Mcl-1蛋白表达水平低于对照组(0.426±0.028)(P均<0.05); 双荧光素酶报告基因实验显示,只有当MAPK4-WT-3' UTR与miR-127-3p mimic共同转染时荧光素酶活性被抑制,这提示miR-127-3p能与MAPK4直接结合,miR-127-3p mimic转染组(0.121±0.003)U251细胞MAPK4蛋白表达水平低于对照组(0.467±0.028)(P<0.05)。结论 miR-127-3p在神经胶质瘤患者脑脊液中呈低表达,上调miR-127-3p能抑制神经胶质瘤U251细胞增殖,促进其凋亡,其机制可能与调控Bcl凋亡相关基因及抑制靶基因MAPK4有关。     

Marsdenia tenacissima extract prevents the malignant progression of glioma through upregulating lncRNA MEG3 and SFRP1-dependent inhibition of Wnt/β-catenin pathway

Background/Aim

Recent studies have highlighted the tumor-suppressive effect of Marsdenia tenacissima extract (MTE) on human cancers. This research unveils the potential impact of MTE on glioma and ascertains the relevant molecular mechanisms.

Methods

Glioma cells were treated with MTE, with normal human astrocytes (NHAs) as controls. A battery of function experiments, including the CCK-8 viability test, colony formation assay, scratch migration assay, and Transwell invasion assay, was executed to address the responses of glioma cells to MTE treatment and gain or loss of function of lncMEG3, miR-542-3p, and SFRP1. FISH, RIP, and dual-luciferase reporter assays were adopted for assessing gene interactions. U251-GFP-Luc cells were delivered into nude mice through intracranial injection to develop an orthotopic glioma model for in vivo validation.

Results

200 mg/mL MTE could suppress the proliferating, migrating, and invading properties of glioma cells but not affect those of NHAs. MTE treatment enhanced the expression of lncMEG3, which competes with SFRP1 for binding miR-542-3p. SFRP1 could inactivate the Wnt/β-catenin pathway. Animal experimentation substantiated the antitumor activity and mechanism of MTE in nude mice.

Conclusions

MTE suppresses glioma via the lncMEG3/miR-542-3p/SFRP1/Wnt/β-catenin axis. These findings contribute to a theoretical basis for the use of MTE for glioma patients.     

lncRNA SNHG7对胶质瘤细胞侵袭、迁移的影响

目的 探讨长链非编码RNA(lncRNA)小核仁RNA宿主基因7(SNHG7)与胶质瘤生存预后的关系,及其对胶质瘤细胞侵袭和迁移的影响。方法 选取2015年6月至2016年3月手术切除的胶质瘤组织80例（术后随访截止2020年4月）和50例颅脑损伤颅内减压术中切取的非肿瘤脑组织为对照,用RT-PCR法检测lncRNA SNHG7的表达水平。体外培养胶质瘤U87细胞,转染不同质粒敲低lncRNA SNHG7表达,用Transwell实验检测细胞侵袭和迁移能力;双荧光素酶报告基因实验检测lncRNA SNHG7对miR-4516的调控作用。结果 胶质瘤组织lncRNA SNHG7表达量明显高于对照组（P<0.05）;多因素Cox回归分析显示,lncRNA SNHG7高表达是胶质瘤病人不良生存预后的独立影响因素（P<0.05）;生存曲线分析显示,高表达组胶质瘤病人中位总生存期较低表达组明显缩短（P<0.05）。敲低lncRNA SNHG7表达,明显抑制U87细胞侵袭和迁移力（P<0.05）。双荧光素酶报告基因实验证实lncRNA SNHG7靶向上调miR-4516表达...     

长链非编码RNA MALAT1对神经母细胞瘤系细胞生物学特性的影响

目的 探讨长链非编码RNA MALAT1对神经母细胞瘤系细胞生物学特性的影响及作用机制。方法 体外培养神经母细胞瘤系SHEP2细胞，细胞分为Control、sh-MALAT1、miR-181a-5p inhibitor和sh-MALAT1+ miR-181a-5p inhibitor组，其中sh-MALAT1组转染sh-MALAT1，miR-181a-5p inhibitor组转染miR-181a-5p inhibitor，sh-MALAT1+inhibitor组共同转染sh-MALAT1与miR-181a-5p inhibitor，Control组加入等量空载体。PCR检测mRNA水平；生物信息预测MALAT1与miR-181a-5p的靶向关系，荧光素酶实验鉴定；CCK8法检测细胞增殖能力；Hoechst法检测细胞凋亡；划痕实验测试细胞迁移；Transwell实验检测细胞侵袭；免疫印迹法检测蛋白表达。结果 sh-MALAT1明显降低MALAT1并提高miR-181a-5p在神经母细胞瘤细胞系SHEP2细胞mRNA水平。miR-181a-5p mimic明显降低MALAT1 wt荧光素酶活性。sh-MALAT1抑制SHEP2细胞增殖、侵袭及迁移，促进细胞凋亡；miR-181a-5p inhibitor促进细胞增殖、侵袭及迁移，抑制细胞凋亡，并减弱sh-MALAT1产生的影响。同时，sh-MALAT1抑制PI3K/Akt信号通路，而miR-181a-5p inhibitor可激活此信号通路并减弱sh-MALAT1的抑制作用。结论 MALAT1靶向下调miR-181a-5p表达促进神经母细胞瘤细胞系SHEP2细胞增殖、迁移和侵袭。     

Clinical and preclinical evaluation of miR-144-5p as a key target for major depressive disorder

Background

Neuronal abnormalities are closely associated with major depressive disorder (MDD). Available evidence suggests a role for microRNAs (miRNAs) in regulating the expression of genes involved in MDD. Hence, miRNAs that can be potential therapeutic targets need to be identified.

Methods

A mouse model of chronic unpredictable stress (CUS) was used to evaluate the function of miRNAs in MDD. miR-144-5p was screened from the hippocampi of CUS mice based on sequencing results. Adenovirus-associated vectors were used to overexpress or knockdown miR-144-5p in mice. BpV(pic) and LY294002 were used to determine the relationship between miR-144-5p target genes PTEN and TLR4 in neuronal impairment caused by miR-144-5p deficiency. Western blotting, immunofluorescence, ELISA immunosorbent assay, and Golgi staining were used to detect neuronal abnormalities. Serum samples from healthy individuals and patients with MDD were used to detect miR-144-5p levels in the serum and serum exosomes using qRT-PCR.

Results

miR-144-5p expression was significantly decreased within the hippocampal dentate gyrus (DG) of CUS mice. Upregulation of miR-144-5p in the DG ameliorated depression-like behavior in CUS mice and attenuated neuronal abnormalities by directly targeting PTEN and TLR4 expression. Furthermore, miR-144-5p knockdown in normal mice led to depression-like behavior via inducing neuronal abnormalities, including abnormal neurogenesis, neuronal apoptosis, altered synaptic plasticity, and neuroinflammation. miR-144-5p deficiency-mediated neuronal impairment was mediated by PI3K/Akt/FoxO1 signaling. Furthermore, miR-144-5p levels were downregulated in the sera of patients with MDD and associated with depressive symptoms. Consistently, serum exosome-derived miR-144-5p levels were decreased in patients with MDD.

Conclusion

miR-144-5p plays a vital role in regulating neuronal abnormalities in depression. Our findings provide translational evidence that miR-144-5p is a new potential therapeutic target for MDD.     

lncRNA MLK7-AS1通过抑制miR-375的表达促进胶质瘤U251细胞的增殖和侵袭

目的 探讨长链非编码RNA（lncRNA）MLK7-AS1在人脑胶质瘤组织中表达及其对胶质瘤U251细胞增殖、侵袭的影响。方法 选择2016~2017年手术切除的脑胶质瘤组织标本45例,2007版WHO分级Ⅰ级8例,Ⅱ级15例,Ⅲ级10例,Ⅳ级12例。另选择其中10例瘤旁正常脑组织作对照。体外培养U251细胞和人正常星形胶质细胞（NHA）。U251细胞根据转染质粒分成四组:转染miR-375 mimic组、转染si-MLK7-AS1组、同时转染miR-375 inhibitor和si-MLK7-AS1组以及只转染miR-375 inhibitor组。RT-qPCR检测MLK7-AS1和miR-375的表达水平;荧光素酶报告基因实验验证MLK7-AS1与miR-375之间的关系;CCK-8法检测U251细胞增殖活性,Transwell实验检测U251细胞侵袭能力。结果 高级别胶质瘤组织MLK7-AS1表达水平明显高于低级别胶质瘤组织（P<0.05）,而后者明显高于瘤旁正常脑组织（P<0.05）;高级别胶质瘤组织miR-375表达水平明显低于低级别胶质瘤组织（P<0.05）,而后者明显低于瘤旁正常脑组织（P<0.05）。U251细胞MLK7-AS1表达水平明显高于NHA（P<0.05）,miR-375表达水平明显低于NHA（P<0.05）。序列分析显示MLK7-AS1和miR-375 存在特异性结合序列,荧光素酶报告基因实验表明U251细胞MLK7-AS1负调控miR-375表达。沉默MLK7-AS1表达通过上调miR-375表达明显抑制U251细胞增殖和侵袭（P<0.05）。结论 lncRN AMLK7-AS1可能通过调节miR-375的表达水平在人脑胶质瘤中发挥着促癌的作用     

胶质瘤组织miR-3653的表达及miR-3653对胶质瘤TG905细胞侵袭、迁移的影响

目的 探讨胶质瘤组织miR-3653表达变化及miR-3653对人胶质瘤TG905细胞侵袭和迁移的影响及其分子机制。方法 收集2017年1月至2019年3月手术切除胶质瘤组织和瘤旁脑组织各25例。体外培养TG905细胞,过表达组转染MiR-3653 mimic质粒,过表达对照组转染NC-MiR-3653 mimic质粒,抑制对照组转染NC-MiR-3653 inhibitor质粒,抑制组转染MiR-3653 inhibitor质粒,miR-3653+ZEB2过表达组同时转染miR-3653 mimic和ZEB2 mimic质粒。利用qRT-PCR及免疫印迹法检测mRNA和蛋白表达;应用Transwell实验和划痕实验检测细胞侵袭和迁移能力。结果 与瘤旁脑组织相比,胶质瘤组织miR-3653表达水平明显降低（P<0.05）。低表达miR-3653显著促进胶质瘤TG905细胞的侵袭及迁移（P<0.05）。过表达miR-3653显著抑制胶质瘤TG905细胞的侵袭及迁移（P<0.05）,明显抑制TG905细胞上皮-间质转化分子和ZEB2的表达（P<0.05）;过表达ZEB2,可有效抑制miR-3653过表达的作用（P<0.05）。结论 胶质瘤组织miR-3653呈低表达,通过靶向上调 ZEB2,促进细胞上皮-间质转化及细胞侵袭、迁移能力。     

miR-181a和miR-181b抑制胶质瘤细胞的增殖和侵袭

目的 探讨miR-181a和miR-181b对胶质瘤细胞增殖和侵袭等影响.方法 通过实时荧光定量PCR检测miR-181a和miR-181b在胶质瘤组织和细胞株中的表达情况.我们合成miR-181a和miR-181b寡聚核苷酸及构建pre-miR-181a和pre-miR-181b表达载体,转染胶质瘤细胞,通过MTT、Transwell实验、流式检测和软琼脂实验,观察上调miR-181a和miR-181b表达后对胶质瘤细胞增殖、侵袭、转化能力和细胞凋亡的影响.结果 miR-181a和miR-181b在胶质瘤组织和细胞株较正常脑组织均呈过低表达;miR-181a表达水平与胶质瘤等级呈负相关.上调miR-181a和miR-181b表达能有效抑制胶质瘤细胞生长,降低其转化和侵袭能力,诱导凋亡.结论 胶质瘤中异常低表达的miR-181a和miR-181b可能发挥着肿瘤抑制因子作用.     

MiR-18a Aggravates Intracranial Hemorrhage by Regulating RUNX1-Occludin/ZO-1 Axis to Increase BBB Permeability

ObjectivesTo study the molecular mechanisms of miR-18a aggravating intracranial hemorrhage (ICH) by increasing the blood-brain barrier (BBB) permeability.MethodsBrain microvascular endothelial cells (BMVECs) and astrocytes were isolated, identified, and co-cultured to establish in vitro BBB model. BMVECs co-cultured with astrocytes were stimulated with or without thrombase and then transfected with miR-18a mimic and/or si-RUNX1. The trans-endothelial electric resistance (TEER) and FlNa flux were measured, respectively. The potential interaction between RUNX1 and miR-18a was also detected. Additionally, SD rats were injected with fresh autologous non-anticoagulant blood into the brain basal ganglia to establish ICH model. After administration with miR-18a, sh-miR-18a, miR-18a+RUNX1, sh-miR-18a+sh-RUNX1, respectively, BBB permeability was assessed.ResultsAfter overexpressing miR-18a, the expression levels of RUNX1, Occludin and ZO-1 were decreased, but the Evan's blue contents and brain water contents were significantly increased in ICH rats. Additionally, rat neurological function was impaired, accompanying with an increase of TEER and fluorescein sodium flux. MiR-18a was a direct target of RUNX1 and it could bind to the promoters of RUNX1 to inhibit the expression of Occuldin and ZO-1. Consistently, these phenomena could also be observed in the corresponding cell model. Conversely, miR-18a knockdown or RUNX1 overexpression just presented an improvement effect on ICH.ConclusionsMiR-18a plays a critical role during ICH because it targets to RUNX1 to inhibit the expression of tight junction proteins (Occludin and ZO-1) and then disrupt BBB permeability. MiR-18a might be a probable therapeutic target for ICH diseases.     

Overexpression of miR-582-5p Inhibits the Apoptosis of Neuronal Cells after Cerebral Ischemic Stroke Through Regulating PAR-1/Rho/Rho Axis

Objective

The purpose of this study was to explore the role of miR-582-5p/proteinase-activated receptors type I (PAR-1)/Rho/Rho in neuronal cell apoptosis after cerebral ischemic stroke (CIS).

miR-6858 plays a key role in the process of melatonin inhibition of the malignant biological behavior of glioma

MicroRNAs (miRNAs), small non-coding RNA molecules with a length of 18–25 nucleotides, have been shown to be involved in mediating various malignant properties of GBM, including growth, invasion and angiogenesis. Here, we investigated whether miRNAs might be involved in mediating the suppression of malignant properties of GBM by melatonin (MEL), an amine hormone secreted by the pineal gland. Sequencing was performed to screen specifically for miRNAs induced by MEL in U87 and an orthotopically xenografted primary GBM cell line, GBM#P3. MiR-6858-5p was the most significantly up-regulated miR in GBM cell lines in response to MEL (~5 × ). Transfection of a mimic of miR-6858-5p into both cell lines led to a decrease in viability of ~ 50% at 72 h, confirming a suppressive role for miR-6858-5p in GBM. In contrast, an inhibitor of miR-6858-5p rescued GBM cells from MEL suppression of proliferation, migration and invasion. Analysis using Targetscan yielded candidate mRNAs targeted by miR-6858-5p, some of which are involved in the SIRT/AKT signaling pathway. In cells transfected with a mimic or an inhibitor of miR-6858-5p, levels of SIRT3 and downstream components of the AKT signaling pathway were suppressed or up-regulated, respectively, both in vitro and in an in vivo orthotopic xenograft model. Our results elucidated a novel molecular mechanism underlying MEL suppression of GBM, highlighting a role for miRNAs, and provide a potential therapeutic strategy for GBM.     

木香烃内酯通过调控LncRNA LINC01116/miR-9-5p的表达来减轻过氧化氢诱导的大鼠脑微血管内皮细胞损伤

目的 探讨木香烃内酯(Cos)对过氧化氢(H₂O₂)诱导的大鼠脑微血管内皮细胞的氧化应激、凋亡的影响及其对长链非编码RNA LINC01116(LncRNA LINC01116)/微小RNA-9-5p(miR-9-5p)的调控作用。方法 原代分离培养大鼠脑微血管内皮细胞,并随机分成Con组、H₂O₂组、Cos-L组、Cos-M组、Cos-H组、Cos-H+pcDNA组、Cos-H+pcDNA-LINC01116组; 采用化学比色法检测丙二醛(MDA)、还原型谷胱甘肽(GSH)的水平及超氧化物歧化酶(SOD)的活性; 流式细胞术检测细胞凋亡率; 实时荧光定量聚合酶链反应(qRT-PCR)检测LINC01116、miR-9-5p的表达水平; 双荧光素酶报告实验验证LINC01116与miR-9-5p的靶向关系; 蛋白免疫印迹法(Western blot)检测B淋巴细胞瘤-2相关蛋白(Bax)、B淋巴细胞瘤-2(Bcl-2)的表达水平。结果 H₂O₂处理后MDA的水平显著升高(P<0.05),GSH水平与SOD活性显著降低(P<0.05),细胞凋亡率显著升高(P<0.05),Bax蛋白水平显著升高(P<0.05),Bcl-2蛋白水平显著降低(P<0.05),LINC01116的表达水平显著升高(P<0.05),miR-9-5p的表达水平显著降低(P<0.05); Cos处理后MDA的水平显著降低(P<0.05),GSH水平与SOD活性显著升高(P<0.05),细胞凋亡率显著降低(P<0.05),Bax蛋白水平显著降低(P<0.05),Bcl-2蛋白水平显著升高(P<0.05),LINC01116的表达水平显著降低(P<0.05),miR-9-5p的表达水平显著升高(P<0.05),且Cos-L组、Cos-M组、Cos-H组上述指标的水平比较均有明显差异(P<0.05); 双荧光素酶报告实验证实LINC01116可靶向结合miR-9-5p; LINC01116过表达可减弱木香烃内酯对H₂O₂诱导的大鼠脑微血管内皮细胞凋亡及氧化应激的作用。结论 木香烃内酯可能通过抑制LINC01116的表达及促进miR-9-5p的表达来抑制H₂O₂诱导的大鼠脑微血管内皮细胞的氧化应激及细胞凋亡,从而减轻细胞损伤。     

急性脑梗死患者血清lncRNA SNHG14和miR-145-5p水平变化及其与疾病发生风险的关系

目的 探讨急性脑梗死患者外周血lncRNA SNHG14和miR-145-5p表达水平变化及其与疾病发生风险的关系。方法 选取本院治疗的135例急性脑梗死患者作为研究对象,另选择同期健康志愿者108例作为对照组; 荧光定量反应(qRT-PCR)检测外周血lncRNA SNHG14和miR-145-5p表达水平; Pearson相关性分析lncRNA SNHG14和miR-145-5p表达水平与病情严重程度的关系; 受试者工作特征(ROC)评估 lncRNA SNHG14和miR-145-5p表达水平对急性脑梗死的诊断价值; Logistic回归分析lncRNA SNHG14和miR-145-5p表达水平与急性脑梗死发生风险的关系。结果 与对照组比较,急性脑梗死患者血清lncRNA SNHG14表达水平升高,miR-145-5p表达水平降低; 随着病情程度的增加,lncRNA SNHG14表达水平逐渐升高,miR-145-5p表达水平逐渐降低(P<0.05)。SNHG14表达水平与患者NIHSS评分呈显著正相关(r=0.416,P=0.000),miR-145-5p表达水平与患者NIHSS评分、SNHG14表达水平均呈显著负相关(r=-0.318,P=0.029; r=-0.487,P=0.000)。lncRNA SNHG14和miR-145-5p表达水平与患者OCSP分型、脑梗死面积、血脂异常有关(P<0.05),lncRNA SNHG14对急性脑梗死诊断的AUC为0.708,敏感性为80.74%,特异性为57.78%; miR-145-5p对急性脑梗死诊断的AUC为0.632,敏感性为77.78%,特异性为50.37%。Logistic多因素回归分析显示血脂异常,lncRNA SNHG14,miR-145-5p表达水平是影响急性脑梗死发生的独立危险因素。结论 急性脑梗死患者外周血lncRNA SNHG14表达水平升高,miR-145-5p表达水平降低,并与患者病情有关,可能是急性脑梗死患者潜在诊断标志物,且是疾病的独立预测因子。     

MiR-342-5p protects neurons from cerebral ischemia induced-apoptosis through regulation of Akt/NF-κB pathways by targeting CCAR2

ObjectivesIschemic stroke causes high morbidity, mortality and health burden in the world. MiR-342-5p was associated with Alzheimer's disease and cardio-protection. Herein, we aimed to reveal effects of miR-342-5p on cerebral ischemia injury as well as novel targets for stroke.Materials and methodsAgomiR-342-5p was intracerebroventricularly injected into the middle cerebral artery occlusion (MCAO) mouse models to evaluate functions of miR-342-5p on cerebral ischemia. RT-qPCR and western blot assays were used to evaluate genes expression. Oxygen-glucose deprivation (OGD) was used as an in vitro model for ischemia. Viability and apoptosis ratio of neurons was evaluated by CCK-8, LDH release detection, and flow cytometry. The potential targets of miR-342-5p were predicted by Targetscan, and their interaction was confirmed by luciferase assay.ResultsThe intervention of miR-342-5p effectively attenuated ischemic injury in MCAO mice. MiR-342-5p overexpression could protect neurons against OGD-induced injury, as revealed by increased cell viability and BCL2 expression, and decreased LDH release, apoptosis ratio, and BAX expression in OGD-induced neurons. Mechanically, miR-342-5p could directly bound with CCAR2 to inhibit its expression. Overexpressing CARR2 aggravated the OGD-induced injury of neurons, which was partly restrained by overexpressing miR-342-5p reversed. Furthermore, miR-342-5p/CARR2 axis regulates Akt/NF-κB signaling pathway in vitro as well as in vivo cerebral ischemia models.ConclusionsMiR-342-5p inhibited neuron apoptosis by regulating Akt/NF-kB signaling pathway via CCAR2 suppression. Our findings revealed the neuroprotection of miR-342-5p in cerebral ischemia.