心肌肥厚大鼠心肌组织及肥大心肌细胞中环状RNA rno_circRNA_016002表达观察

目的 观察心肌肥厚大鼠心肌组织及肥大心肌细胞中环状RNA rno_circRNA_016002的表达变化,并探讨其在心肌肥厚过程中的作用.方法 将12只SD大鼠随机分为Control组与异丙肾上腺素(ISO)组,每组6只.ISO组每天腹腔注射ISO 3 mg/kg,Control组注射同等体积的生理盐水,连续注射两周后...     

丹参酮通过抑制miR-376b-5p逆转自发性高血压大鼠左室重构

目的探讨miR-376b-5p在丹参酮逆转老年自发性高血压大鼠(SHR)左室重构中的作用。方法将60只17月龄的SHR随机分为对照组、丹参酮组和丹参酮+miR-376b-5p组(n=20),其中丹参酮组和丹参酮+miR-376b-5p组接受5 ml·kg~(-1)·d~(-1)的丹参酮ⅡA磺酸钠注射液灌胃处理,连续12 w;此外,丹参酮+miR-376b-5p组尾静脉注射过表达miR-376b-5p的慢病毒载体,对照组接受5 ml·kg~(-1)·d~(-1)的生理盐水灌胃处理。12 w后分离右侧颈总动脉,采用Power Lab生物信号记录分析系统分析血压及血流动力学指标〔左心室收缩压(LVSP)、左心室舒张末压(LVEDP)和左心室压力上升/下降最大速率(±dp/dtmax)〕,称量体质量及左心室质量并计算左心室质量指数。取左心室中部冠状切面石蜡切片行HE染色、Masson染色以评估左室重构情况(心肌细胞直径、心肌间质纤维化指数和心肌血管周围纤维化指数)。结果与对照组相比,丹参酮组的收缩压、舒张压、平均动脉压及LVSP和LVEDP均降低,±dp/dt max均升高(P0.05);丹参酮组的左心室质量、左心室质量指数、心肌细胞直径、心肌间质纤维化指数及心肌血管周围纤维化指数均低于对照组。miR-376b-5p过表达后可消除丹参酮对SHR血压及左心室重构的保护效果,丹参酮+miR-376b-5p组的以上指标与对照组均无统计学差异(P0.05)。结论丹参酮对老年SHR左室重构有保护作用,而过表达miR-376b-5p可消除丹参酮对老年SHR左室重构的逆转作用,提示丹参酮可能通过降低miR-376b-5p水平发挥对老年SHR左室重构的保护作用。     

胆酸通过上调miR-23b-3p抑制载脂蛋白A表达

目的分析胆酸降载脂蛋白A(Apo A)效应与miR-23b-3p的关系,研究胆酸降Apo A作用新机制。方法首先用生物信息学在线工具对miR-23b-3p与调控LPA基因的转录因子肝细胞核因子4γ(HNF4γ)进行靶基因分析,使用荧光素酶报告系统对miR-23b-3p与调控LPA基因的转录因子HNF4γ进行靶基因验证实验,Western blot检测Apo A表达水平、p38MAPK(MAPK:丝裂原活化蛋白激酶)及p-p38MAPK,实时定量PCR检测miR-23b-3p表达水平。结果生物信息学分析表明HNF4γ可作为miR-23b-3p的靶基因,荧光素酶报告系统转染miR-23b-3p处理组细胞裂解后荧光强度显著低于对照组,验证了HNF4γ可作为miR-23b-3p的靶基因。胆酸呈剂量和时间依赖性抑制Hep G2细胞Apo A的表达,以32 mg/L和24 h的作用最显著。胆酸抑制Apo A表达与活化MAPK和上调miR-23b-3p有关。结论胆酸呈剂量和时间依赖性地下调Hep G2细胞Apo A表达水平;胆酸降Apo A与上调miR-23b-3p有关。     

长链非编码RNA GAS5通过调控miR-196 b-5 p抑制非小细胞肺癌细胞增殖侵袭迁移的机制

目的 研究长链非编码RNA(LncRNA)GAS5对非小细胞肺癌细胞增殖、迁移和侵袭的影响,探讨其作用机制.方法 运用qRT-PCR检测非小细胞肺癌细胞A549和肺支气管正常细胞16HBE中LncRNA GAS5、miR-196b-5p的表达;将miR-196b-5p组(转染miR-196b-5p mimics)、mi...     

维持性血液透析患者外周血miR-125b-5p与冠状动脉钙化相关性研究

目的 分析外周血miR-125b-5p水平与尿毒症患者冠状动脉钙化严重程度的相关性,并对机制进行探讨。方法 选取2021年1月至2023年5月于武汉市第四医院古田院区接受维持性血液透析的患者为研究对象。所有入选者均接受胸部心脏CT检查,并检测外周血miR-125b-5p水平。在小鼠胸主动脉平滑肌细胞中,探索高磷及miR-125b-5p表达对细胞钙化沉积和炎症蛋白表达的影响。结果 共有117例患者纳入研究,男性69例(59%),女性48例(41%),平均年龄62岁。依据冠状动脉钙化积分将纳入患者分组：轻度冠状动脉钙化(积分<400分)组(71例),严重冠状动脉钙化(积分≥400分)组(46例)。多因素二元logistic回归分析表明外周血miR-125b-5p水平(OR=0.325,95%CI:0.205～0.517,P<0.001)与冠状动脉钙化严重程度独立相关。受试者操作特征曲线分析miR-125b-5p对严重冠状动脉钙化的预测价值,曲线下面积为0.831(95%CI:0.750～0.894,P<0.001)。细胞实验结果显示,相较于对照组,高磷干预下胸主动脉平滑肌...     

急性胰腺炎患者血清miR-148a-3p和miR-551b-3p的表达水平及其临床价值

目的:探讨AP患者血清miR-148a-3p和miR-551b-5p的表达水平及其临床价值。方法:选取2017年1月至2020年9月间儋州市人民医院收治的152例AP患者的临床资料,根据病情严重程度将患者分为MAP组(70例)、MSAP组(40例)和SAP组(42例),SAP组又根据患者预后情况分成生存组(25例)和死...     

心肌肥厚小鼠心肌组织中环状RNA的表达谱分析

目的探索心肌肥厚时环状RNA(circRNA)差异表达的情况及其影响的病理生理进程。方法 SPF级C57BL/6J雄性小鼠6只, 8～10周龄, 按照随机数字表法分为主动脉弓缩窄(TAC)组(n=3)和假手术组(n=3)。通过TAC术建立心肌肥厚小鼠模型。术后4周, 采用高通量测序分析检测TAC组与假手术组小鼠左心室心肌组织差异表达的circRNA, 并采用R语言软件对circRNA进行主成分分析。通过GO和KEGG 2个数据库进行富集分析推测差异表达circRNA来源基因的基本功能及其参与的生物学通路。采用实时荧光定量聚合酶链反应验证测序结果中差异表达的circRNA。结合差异表达的circRNA和TargetScan预测的微小RNA(miRNA)位点, 应用Cytoscape软件构建circRNA-miRNA网络图以预测他们的相互作用。结果对TAC组和假手术组小鼠6个样本中检测到的4 580个circRNA进行主成分分析, R语言软件结果提示前3个主成分, 即第1、2和3主成分的方差贡献率分别为91.01%、3.19%和2.01%, 三者累计方差贡献率为96.21%。在差异表达的c...     

外周血miR-338-5p、miR-140-5p在HBV相关肝细胞癌患者中表达水平及临床意义

目的?探讨外周血血清中微小RNA（microRNA, miR）-338-5p、miR-140-5p在HBV相关肝细胞癌患者中表达水平及临床意义。方法?选取2017年11月—2020年11月我院收治的HBV相关肝细胞癌患者95例作为肝细胞癌组,另选取同时期HBV相关良性肝病患者100例作为良性组,及健康体检者100例作为对照组。采用实时荧光定量PCR检测外周血血清中miR-338-5p、miR-140-5p表达水平及HBV DNA载量,采用Pearson相关分析分析HBV相关肝细胞癌患者外周血血清中miR-338-5p、miR-140-5p表达水平与HBV DNA载量的关系,采用多因素Logistic回归模型分析影响HBV相关肝细胞癌发生的危险因素;ROC曲线分析miR-338-5p、miR-140-5p、异常凝血酶原-Ⅱ（abnormal prothrombin-Ⅱ, PIVKA-Ⅱ）表达对HBV相关肝细胞癌的诊断价值。结果?外周血血清中miR-338-5p、PIVKA-Ⅱ表达水平从高至低依次为肝细胞癌组[（2.73±0.88）、（103.14,319.19）mAU/ml]、良性组[（1.48±0.40）、（32.70,87.15）mAU/ml]、对照组[（1.00±0.27）、（10.36,16.82）mAU/ml],外周血血清中miR-140-5p表达水平从高至低依次为对照组（1.00±0.25）、良性组（0.72±0.20）、肝细胞癌组（0.38±0.12）,两两比较差异均具有统计学意义（P均＜0.05）;肝细胞癌组患者HBV DNA载量（144.97±47.32）明显高于良性组（75.66±21.91）（P＜0.05）。不同TNM分期患者间比较,外周血血清中miR-338-5p、PIVKA-Ⅱ表达水平及HBV DNA载量从高至低依次为TNM Ⅳ期、Ⅲ期、Ⅱ期、Ⅰ期,外周血血清中miR-140-5p表达水平从高至低依次为TNM Ⅰ期、Ⅱ期、Ⅲ期、Ⅳ期,两两比较差异均有统计学意义（P均＜0.05）。HBV相关肝细胞癌患者外周血血清中miR-338-5p表达水平与HBV DNA载量呈正相关（P＜0.05）,而miR-140-5p表达水平与HBV DNA载量呈负相关（P＜0.05）。HBV相关肝细胞癌发生与患者有无糖尿病史、有无长期饮酒史、HBV DNA载量及外周血血清中miR-338-5p、miR-140-5p、PIVKA-Ⅱ表达水平有关（P均＜0.05）。多因素Logistic回归分析显示外周血血清中PIVKA-Ⅱ＞40 mAU/ml、miR-338-5p高表达、miR-140-5p低表达是影响HBV相关肝细胞癌发生的独立危险因素（P＜0.05）。外周血血清中miR-338-5p、miR-140-5p、PIVKA-Ⅱ表达水平联合诊断HBV相关肝细胞癌的AUC为0.930,明显高于3指标单独诊断的AUC（P均＜0.05）,联合诊断的敏感度为98.90%,特异度为87.00%。结论?HBV相关肝细胞癌患者外周血血清中miR-338-5p高表达,miR-140-5p低表达,2者可作为评估HBV相关肝细胞癌发生的血清指标,2者联合PIVKA-Ⅱ更有利于诊断HBV相关肝细胞癌。     

老年肺癌患者外周血Gm31083和miR-450b-5p表达及其与预后的关系

目的 探讨老年肺癌患者外周血Gm31083和微小RNA(miR)-450b-5p表达及其与预后的关系。方法 选择老年肺癌患者120例为研究组;另选择老年健康体检者102例为对照组。采用实时荧光定量-聚合酶链反应(qRT-PCR)测定外周血Gm31083和miR-450b-5p mRNA表达。随访至2021年12月,记录患者总生存期(OS)。比较两组Gm31083和miR-450b-5p mRNA表达;不同病理特征Gm31083和miR-450b-5p mRNA表达;预后与Gm31083 mRNA、miR-450b-5p mRNA表达关系。采用多因素Logistic回归分析影响老年肺癌患者预后危险因素。结果 研究组Gm31083 mRNA表达显著高于对照组,而miR-450b-5p mRNA表达显著低于对照组(P<0.05)。不同性别、年龄、体重指数、肿瘤直径和分化程度Gm31083和miR-450b-5p mRNA表达比较无明显差异(P>0.05);Ⅲ～Ⅳ期Gm31083 mRNA表达显著高于Ⅰ～Ⅱ期,且淋巴结转移Gm31083 mRNA表达显著高于无淋巴结转移(P<...     

miR-376b-3p通过靶向FGF21加重缺氧复氧心肌细胞的损伤

目的 探讨miR-376b-3p对缺氧复氧(H/R)心肌细胞增殖、凋亡的影响及机制。方法 培养心肌细胞H9c2,缺氧复氧法体外模拟H/R细胞损伤,建立心肌细胞损伤模型。用流式细胞术、免疫印迹(Western blot)、酶联免疫吸附(ELISA)检测正常对照组、H/R组、anti-miR-NC组、anti-miR-376b-3p组、anti-miR-376b-3p+si-NC组、anti-miR-376b-3p+si-成纤维细胞生长因子21(FGF21)组细胞凋亡率、凋亡相关蛋白B淋巴细胞瘤2基因(Bcl-2)、Bcl-2相关X蛋白(Bax)表达和肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素17(IL-17)情况。双荧光素酶报告基因实验检测细胞的荧光活性。结果 成功建立缺氧复氧损伤的细胞模型;模型组细胞中miR-376b-3p表达显著升高,FGF21表达显著降低,并且抑制miR-376b-3p可以减轻损伤细胞的凋亡和TNF-α、IL-6、IL-17的含量,以及上调Bcl-2,下调Bax。此外,miR-376b-3p还可靶向FGF21 mRNA。抑制FGF21后,抑制miR-376b-3p对缺氧复氧损伤的H9c2细胞的保护作用被减弱。结论 miR-376b-3p可促进缺氧复氧心肌细胞的凋亡和炎性反应,其机制与靶向FGF21 mRNA相关。     

Circular RNA circVAPA promotes chemotherapy drug resistance in gastric cancer progression by regulating miR-125b-5p/STAT3 axis

BACKGROUND Gastric cancer(GC)is a prevalent malignancy,leading to a high incidence of cancer-associated death.Cisplatin(DDP)-based chemotherapy is the principal therapy for clinical GC treatment,but DDP resistance is a severe clinical challenge and the mechanism remains poorly understood.Circular RNAs(circRNAs)have been identified to play crucial roles in modulating the chemoresistance of gastric cancer cells.AIM To explore the effect of circVAPA on chemotherapy resistance during GC progression.METHODS The effect of circVAPA on GC progression and chemotherapy resistance was analyzed by MTT assay,colony formation assay,Transwell assay,wound healing assay,and flow cytometry analysis in GC cells and DDP resistant GC cell lines,and tumorigenicity analysis in nude mice in vivo.The mechanism was investigated by luciferase reporter assay,quantitative real-time PCR,and Western blot analysis.RESULTS CircVAPA expression was up-regulated in clinical GC tissues compared with normal samples.CircVAPA depletion inhibited proliferation,migration,and invasion and increased apoptosis of GC cells.The expression of circVAPA,STAT3,and STAT3 downstream genes was elevated in DDP resistant SGC7901/DDP cell lines.CircVAPA knockdown attenuated the DDP resistance of GC cells.Mechanically,circVAPA was able to sponge miR-125b-5p,and miR-125b-5p could target STAT3 in the GC cells.MiR-125b-5p inhibitor reversed circVAPA depletion-enhanced inhibitory effect of DDP on GC cells,and STAT3 knockdown blocked circVAPA overexpression-induced proliferation of DDPtreated SGC7901/DDP cells.The depletion of STAT3 and miR-125b-5p inhibitor reversed circVAPA depletion-induced GC cell apoptosis.Functionally,circVAPA contributed to the tumor growth of SGC7901/DDP cells in vivo.CONCLUSION CircVAPA promotes chemotherapy resistance and malignant progression in GC by miR-125b-5p/STAT3 signaling.Our findings present novel insights into the mechanism by which circVAPA regulates chemotherapy resistance of GC cells.CircVAPA and miR-125b-5p may be considered as the potential targets for GC therapy.     

Silencing LncRNA-DANCR attenuates inflammation and DSS-induced endothelial injury through miR-125b-5p

BackgroundLncRNA-DANCR is involved in inflammation and acts as a major contributor to colon cancer. The effects and mechanism of LncRNA-DANCR were first investigated in a DSS-induced colitis model in vivo and vitro.Material and methodsSprague-Dawley rats were given DSS to induce the colitis model. TNF-α, IL-1β, IL-6 levels and expression of intestinal adhesion proteins ZO-1 and MUC2 in colon tissues and DSS-induced NCM460 cells were measured using corresponding kits. A hematoxylin and eosin (H&E) staining assay was performed to evaluate colon tissue pathology conditions. Protein expression levels in DSS-induced NCM460 cells were evaluated by Western blotting, and cell apoptosis was detected using a TUNEL assay. Gene levels in DSS-induced NCM460 cells were evaluated by PCR. The StarBase online tool was used to predict the LncRNA-DANCR target. The LncRNA-DANCR target was verified using a luciferase reporter assay.ResultsLncRNA-DANCR was up-regulated in DSS-induced groups of rats. TNF-α, IL-1β and IL-6 expression was significantly increased in DSS-induced groups of rats and cells. Zo-1 and MUC2 expression levels were decreased in DSS-induced groups of rats. Silencing LncRNA-DANCR reduced inflammation, cell apoptosis and up-regulated ZO-1, MUC2 and Claudin-1 in DSS-induced cells. MiR-125b-5p was the downstream LncRNA-DANCR target. All LncRNA-DANCR effects in the colitis model were reversed by the miR-125b-5p inhibitor.ConclusionLncRNA-DANCR/miR-125b-5p, which may act as a regulatory axis in inflammation, apoptosis and barrier function dysregulation, can provide an essential reference for the development of new drugs in colitis treatment.     

Circular RNA AKT3 governs malignant behaviors of esophageal cancer cells by sponging miR-17-5p

BACKGROUND Recent studies have demonstrated that circular RNA AKT3(circAKT3)plays a crucial role in regulating the malignant phenotypes of tumor cells.However,the potential effects of circAKT3 on esophageal cancer have not been investigated.AIM To illuminate the role of circAKT3 in malignant behaviors of esophageal cancer cells and its underlying mechanism.METHODS Clinical samples were collected to detect the expression of circAKT3.The role of circAKT3 in proliferation,migration,invasion,and apoptosis of esophageal cancer cells was evaluated using Cell Counting Kit-8,wound healing assays,Transwell assays,and fluorescence analysis,respectively.The target of circAKT3 was screened and identified using an online database and luciferase reporter assay.A xenograft nude mouse model was established to investigate the role of circAKT3 in vivo.RESULTS In vitro assays showed that proliferative,migratory,and invasive capacities of esophageal cancer cells were significantly enhanced by circAKT3 overexpression.Furthermore,miR-17-5p was screened as the target of circAKT3,and miR-17-5p antagonized the effects of circAKT3 on esophageal cancer cells.Moreover,we identified RHOC and STAT3 as the direct target molecules of miR-17-5p,and circAKT3 facilitated expression of RHOC and STAT3 by inhibiting miR-17-5p.In vivo assays showed circAKT3 knockdown inhibited growth of esophageal cancer.CONCLUSION CircAKT3 contributed to the malignant behaviors of esophageal cancer in vitro and in vivo by sponging miR-17-5p thus providing a potential target for treatment of esophageal cancer.     

CircRNA_0084927 promotes colorectal cancer progression by regulating miRNA-20b-3p/glutathione S-transferase mu 5 axis

BACKGROUNDColorectal cancer (CRC) is the third most common cancer and the second most common cause of cancer-related death worldwide. The 5-year survival rate of patients with early-stage CRC could reach 90%, but it is very low in patients with advanced-stage CRC. Recent studies have shown that circular RNAs play important roles in regulating the migration and invasion of CRC cells.AIMTo elucidate the role of circRNA_0084927 (circ_0084927) in the migration and invasion of CRC cells and its underlying mechanism.METHODSClinical tissue samples and cells were collected, and the expression of circ_0084927 was detected by quantitative polymerase chain reaction (qPCR). The diagnostic performance of circ_0084927 was assessed by receiver operating characteristic curve analysis. The role of circ_0084927 in CRC cell proliferation, migration, and invasion was determined using cell counting kit-8 assay, wound healing assay, and transwell assay, respectively. The regulatory relationship among circ_0084927, miRNA-20b-3p (miR-20b-3p), and glutathione S-transferase mu 5 (GSTM5) was identified using databases, luciferase reporter assay, qPCR, and Western blot analysis. AKT-mTOR signaling was also verified after circ_0084927 knockdown or miR-20b-3p mimic treatment.RESULTSThe expression of circ_0084927 was significantly increased in CRC tissues and cells, and it was higher in advanced-stage CRC compared with early-stage CRC. The area under the curve (AUC) of circ_0084927 was 0.806 [95% confidence interval (CI): 0.683-0.896]. In addition, the AUC was 0.874 (95%CI: 0.738-0.956) in patients with advanced-stage CRC and 0.713 (95%CI: 0.555-0.840) in those with early-stage CRC. Knockdown of circ_0084927 inhibited the migration and invasion of HCT116 cells. Moreover, circ_0084927 was found to act as a sponge of miR-20b-3p. MiR-20b-3p activation reduced the circ_0084927 level, whereas miR-20b-3p inhibition increased the circ_0084927 level. But the effect was not found after circ_0084927 mutation. In addition, miR-20b-3p expression in CRC patients was also reduced and negatively correlated with circ_0084927 expression. The function of circ_0084927 in HCT116 cells with circ_0084927 knockdown was rescued by miR-20b-3p. Moreover, GSTM5 expression was significantly decreased after overexpressing miR-20b-3p or inhibiting circ_0084927, but its expression was rescued when circ_0084927 and miR-20b-3p were both inhibited. Finally, AKT-mTOR signaling was markedly regulated by circ_0084927 and miR-20b-3p.CONCLUSIONThe expression of circ_0084927 is significantly increased in CRC and higher in advanced-stage CRC than in early-stage CRC. Moreover, circ_0084927 potentially regulates CRC cell migration and invasion via the miR-20b-3p/GSTM5/ AKT/mTOR pathway.     

miR-499a-5p通过靶向APC减轻氧化应激对心肌细胞的损伤

目的研究miR-499a-5p对过氧化氢(H_2O_2)诱导的心肌细胞H9c2增殖、凋亡的影响,并探讨其作用机制。方法用细胞计数试剂盒(CCK-8)检测不同浓度H_2O_2(100、200、400、800μmol/L)处理6 h的H9c2细胞的存活率,筛选400μmol/L H_2O_2处理的H9c2细胞作为模型组。将模型组细胞分为miR-NC组、miR-499a-5p组、si-NC组、si-APC组、miR-499a-5p+pcDNA组、miR-499a-5p+pcDNA-APC组,用流式细胞术、免疫印迹(Western blot)、酶联免疫吸附试验(ELISA)检测各组细胞的存活率、凋亡率、活性氧(ROS)、超氧化物歧化酶(SOD)、丙二醛(MDA)及增殖凋亡相关蛋白增殖细胞核抗原(PCNA)、细胞周期蛋白依靠性激酶抑制剂(P21)、B淋巴细胞瘤-2基因(Bcl-2)、Bcl-2相关的X基因(Bax)的表达。结果 H_2O_2(100、200、400、800μmol/L)呈浓度依赖性抑制H9c2细胞的存活,最适浓度为400μmol/L。模型组细胞中miR-499a-5p表达显著降低,APC表达显著升高;过表达miR-499a-5p、抑制APC均可明显减轻H_2O_2诱导的H9c2细胞的增殖抑制、凋亡促进和氧化应激作用,并且miR-499a-5p还可靶向抑制APC。过表达APC逆转了miR-499a-5p对H_2O_2诱导的心肌细胞损伤。结论 miR-499a-5p可调控H_2O_2诱导的心肌细胞增殖、凋亡和氧化应激,其机制与靶向抑制APC有关,将可为氧化应激引起的心肌细胞损伤的治疗提供新靶点。     

CircRNA-001241 mediates sorafenib resistance of hepatocellular carcinoma cells by sponging miR-21-5p and regulating TIMP3 expression

Hepatocellular carcinoma (HCC) is one of the major malignancies worldwide and its incidence is on the rise, closely related to advanced liver disease. Sorafenib chemotherapy is one of the main treatment options for patients with advanced HCC. Despite several reports on HCC multidrug resistance, the underlying regulatory mechanisms are still unclear. In this study, we found circ-001241 was significantly upregulated in HCC tissues and cells. Knockdown of circ-001241 markedly inhibited HCC cell proliferation and decreased sorafenib-resistance. More importantly, circRNA acts as a ceRNA to suppress the expression and activity of miR-21-5p, leading to the increase in TIMP3 expression. In addition, circRNA-001241 facilitated HCC sorafenib-resistance by regulating the miR-21-5p/TIMP3 axis. Taken together, our study elucidated the oncogenic role of circ-001241 in mediating sorafenib resistance in HCC, providing insights and opportunities to overcome sorafenib resistance in patients with advanced hepatocellular carcinoma.     

血清miR-92a-1-5p及miR-92a-2-5p表达水平与老年卒中后抑郁的关系

目的 分析血清微小核糖核酸-92a-1-5p ( miR-92a-1-5p)、 miR-92a-2-5p 表达水平与老年卒中后抑郁的关系.方法 选取2018年2月至2020年10月胶州中心医院收治的129例老年卒中患者为研究组,另选取110名同期健康体检者为对照组,均检测血清miR-92a-1-5p、miR-92a-2...