MiR-92a-3p_R+1和miR-92a-1-5p在ox-LDL诱导大鼠VSMC表型转化和增殖中的作用

目的探讨miR-92a-3p_R+1和miR-92a-1-5p在氧化型低密度脂蛋白(ox-LDL)诱导大鼠血管平滑肌细胞(VSMC)表型转化和增殖中的作用及其与ERK1/2信号通路的相关性。方法分离、培养大鼠VSMC,以ox-LDL(50 mg/L)诱导VSMC,采用ERK1/2特异性抑制剂U0126(10μmol/L)阻断ox-LDL(50 mg/L)诱导VSMC的ERK1/2信号激活,MicroRNA微阵列分析VSMC的miR-92a-3p_R+1和miR-92a-1-5p表达,CCK-8法和Brdu流式细胞术检测细胞增殖;免疫荧光法检测VSMC收缩表型标志蛋白SM22α的变化;Western blot检测VSMC的ERK1/2通路信号激活情况(ERK、p-ERK)、表型标志蛋白SM22α、细胞周期相关蛋白(PCNA、cyclin D1、p21、p27)的表达情况。结果 ox-LDL诱导下,VSMC的miR-92a-3p_R+1和miR-92a-1-5p表达明显上调,VSMC的ERK1/2磷酸化水平明显增加,SM22α的表达降低,同时细胞周期相关蛋白PCNA、cyclin D1高表达,p21、p27低表达;ERK1/2通路特异性抑制剂U0126干预后,ERK1/2磷酸化水平受抑制,相应的VSMC miR-92a-3p_R+1和miR-92a-1-5p表达明显下调(P0.05),VSMC增殖显著下降,SM22α的表达上调(P0.05),提示VSMC由合成表型转化为收缩表型,并下调PCNA、cyclin D1的表达,上调p21、p27蛋白的表达(P0.05),说明其表型转化和增殖明显受抑制。结论 miR-92a-3p_R+1和miR-92a-1-5p在ox-LDL诱导VSMC表型转化和增殖中起重要作用,并与ERK1/2信号通路密切相关。     

血浆miR-1228-5p、miR-34a-5p、miR-192-5p和miR-30a-3p水平与早发冠心病的相关性及其初筛价值

目的]探讨血浆miR-1228-5p、miR-34a-5p、miR-192-5p和miR-30a-3p水平与早发冠心病(PCAD)的相关性及其对PCAD的初筛价值。[方法]根据纳入标准及排除标准,纳入6例明确诊断的PCAD患者作为PCAD组,纳入6例健康受试者作为对照组,收集PCAD组和对照组血液,提取血清样本并保存,使用DNBseq平台检测两组血清中miRNA水平,筛选差异水平显著的miRNA。根据纳入标准及排除标准,收集78例PCAD患者、75例晚发冠心病患者和69例健康对照者的血液并对筛选的miRNA进行实时荧光定量PCR验证。分析PCAD患者冠状动脉造影报告,采用Gensini评分评估冠状动脉病变的严重程度。Spearman相关性检验分析有关miRNA水平与冠状动脉狭窄程度的相关性。ROC曲线分析血浆miR-1228-5p、miR-34a-5p、miR-192-5p及miR-30a-3p水平对PCAD的诊断价值,多因素Logistic回归分析PCAD发生的影响因素。[结果]DNBseq平台分析显示,差异表达miRNA 33个,其中上调miRNA 17个,下调miRNA 16个,差异水平最为显著的5个miRNA分别为miR-1228-5p、miR-34a-5p、miR-192-5p、miR-424-3p和miR-30a-3p;实时荧光定量PCR结果显示,与对照组相比,PCAD患者血浆miR-1228-5p升高1.7倍,miR-34a-5p升高1.4倍,miR-192-5p升高0.7倍,miR-30a-3p升高2.5倍(P＜0.05),两组间血浆miR-424-3p水平差异无统计学意义(P＞0.05);血浆miR-1228-5p和miR-34a-5p水平与PCAD患者冠状动脉狭窄程度均呈正相关(r＝0.307,P＝0.004;r＝0.238,P＝0.036);ROC曲线分析显示,miR-1228-5p、miR-34a-5p、miR-192-5p和miR-30a-3p诊断PCAD的ROC曲线下面积分别为0.903、0.832、0.731及0.798,其联合诊断PCAD的ROC曲线下面积为0.990,95%CI为0.976～1.000。[结论]PCAD患者血浆miR-1228-5p、miR-34a-5p、miR-192-5p和miR-30a-3p水平显著升高,其联合检测诊断PCAD具有较高的准确性,有望成为初筛PCAD的新型生物标志物。     

下调miR-92a通过调控PIAS3抑制ox-LDL诱导RAW264.7细胞炎症介质分泌和脂质蓄积

目的探讨下调miR-92a对氧化型低密度脂蛋白(ox-LDL)诱导RAW264.7细胞炎症介质分泌和脂质蓄积的影响及其机制。方法以不同浓度(0、25、50、100 mg/L)的ox-LDL处理RAW264.7细胞24 h或以100 mg/L ox-LDL分别处理RAW264.7细胞0、12、24 h后,采用定量实时聚合酶链反应(qRT-PCR)检测ox-LDL对miR-92a表达的影响。建立miR-92a低表达的RAW264.7细胞株,并给予100 mg/L ox-LDL处理后,用qRT-PCR、油红O染色、一氧化氮(NO)荧光探针(DAF-FMDA)和Western blot检测下调miR-92a表达对ox-LDL诱导的RAW264.7细胞中炎症因子诱导型一氧化氮合酶(i NOS)、白细胞介素6(IL-6)和IL-1β表达、脂质蓄积以及信号转导子和转录激活子3(STAT3)信号通路相关蛋白p-STAT3、STAT3蛋白表达的影响。建立活化STAT3蛋白抑制分子(PIAS3)和miR-92a低表达的RAW264.7细胞株,并给予100 mg/L ox-LDL处理后,观察沉默PIAS3表达对ox-LDL作用下miR-92a低表达的RAW264.7细胞中炎症因子、脂质蓄积以及STAT3信号通路的影响。Target Scan软件预测和双荧光素酶报告实验验证miR-92a和PIAS3的靶向关系。结果随着ox-LDL作用时间和浓度的增加,RAW264.7细胞中miR-92a表达升高;双荧光素酶报告实验验证PIAS3是miR-92a的靶基因。采用ox-LDL处理后RAW264.7细胞中miR-92a、i NOS、IL-6、IL-1β、p-STAT3表达升高,NO释放增多和细胞内脂滴升高,而PIAS3的表达下降。这种调控作用可被anti-miR-92a所抑制;而沉默PIAS3后,anti-miR-92a的这一抑制作用得以恢复。结论下调miR-92a可通过调控PIAS3抑制ox-LDL诱导RAW264.7细胞炎症介质分泌和脂质蓄积。     

lncRNA PCAT19靶向miR-143-3p通过信号通路PI3K/Akt对甲状腺癌细胞增殖和凋亡的影响及机制

目的探讨lncRNA PCAT19对甲状腺癌细胞增殖和凋亡的影响及作用机制。方法实验分为miR-con组、miR-143-3p组、si-con组、si-PCAT19组、pcDNA组、pcDNA-PCAT19组、si-PCAT19+anti-miR-con组、si-PCAT19+anti-miR-143-3p组、miR-con+WT-PCAT19组、miR-con+MUT-PCAT19组、miR-143-3p+WT-PCAT19组、miR-143-3p+MUT-PCAT19组。qRT-PCR检测miR-143-3p和PCAT19的表达水平;Western印迹检测蛋白表达;MTT法检测细胞存活率;流式细胞术检测细胞凋亡;双荧光素酶报告实验检测PCAT19和miR-143-3p的靶向关系。结果相较于正常甲状腺细胞HT-ori3,甲状腺癌细胞BCPAP、TPC-1、SW1736中PCAT19的表达水平显著升高,miR-143-3p的表达水平显著降低(P<0.05)。敲低PCAT19和高表达miR-143-3p抑制甲状腺癌细胞BCPAP增殖,促进细胞凋亡;促进裂解的半胱氨酸天冬氨酸蛋白酶(Cleaved-caspase)-3蛋白的表达,抑制细胞周期蛋白(Cyclin)D1的表达。PCAT19靶向负调控miR-143-3p,miR-143-3p低表达可以部分逆转PCAT19低表达对BCPAP细胞增殖抑制和凋亡促进的作用。敲低PCAT19抑制p-AKT和磷脂酰肌醇3-激酶的p1102催化亚基(PI3Kp110α)的表达,miR-143-3p低表达可逆转PCAT19低表达对p-AKT和PI3Kp110α的抑制作用。结论lncRNA PCAT19可抑制甲状腺癌细胞增殖,促进其凋亡,其机制可能与miR-143-3p及PI3K/AKT信号通路有关。     

帕金森病患者血清miR-103a-3p、miR-486-5p水平变化及临床意义

目的 探讨帕金森病(PD)患者血清miR-103a-3p、miR-486-5p水平变化及临床意义.方法 选取183例PD患者为PD组,根据Hoehn-Yahr分级分为重度组(n=53)、中度组(n=71)、轻度组(n=59),另选取75例体检健康者为对照组.采用qRT-PCR检测血清miR-103a-3p、miR-48...     

Remote ischemic preconditioning protects against cerebral ischemia injury in rats by upregulating miR-204-5p and activating the PINK1/Parkin signaling pathway

Metabolic Brain Disease - Remote ischemic preconditioning (RiPC) is the process where preconditioning ischemia protects the organs against the subsequent index ischemia. RiPC is a protective method...     

结核潜伏感染者全血miR-144-3p、miR-146a-5p的表达

目的探讨结核潜伏感染者全血miR-144-3p、miR-146a-5p的表达及其与活动性肺结核患者的差异。方法收集结核潜伏感染者30例,活动性肺结核患者30例。收集全血,提取总RNA,利用反转录-荧光定量PCR方法检测miR-144-3p、miR-146a-5p的表达。两组间比较采用t检验。结果结核潜伏感染者全血中miRNA144-3p的表达(2.014±1.48)比活动性肺结核患者(1.056±0.746)明显提高,差异有统计学意义(P<0.05),而结核潜伏感染者全血中miR-146a-5p的表达(1.937±1.109)与活动性肺结核患者(1.469±0.693)相似,差异无统计学意义(P>0.05)。结论 miR-144-3p可能成为诊断结核潜伏感染者的标志物。     

Down-regulation of mi R-30a-3p/5p promotes esophageal squamous cell carcinoma cell proliferation by activating the Wnt signaling pathway

AIM To investigate the potential role of micro RNA-30 a(mi R-30 a) in esophageal squamous cell carcinoma(ESCC).METHODS Expression of mi R-30 a-3 p/5 p was analyzed using microarray data and fresh ESCC tissue samples. Both in vitro and in vivo assays were used to investigate the effects of mi R-30 a-3 p/5 p on ESCC cell proliferation. Furthermore,Kyoto Encyclopedia of Genes and Genomes analysis was performed to explore underlying mechanisms involved in ESCC,and then,assays were carried out to verify the potential molecular mechanism of mi R-30 a in ESCC.RESULTS Low expression of mi R-30 a-3 p/5 p was closely associated with advanced ESCC progression and poor prognosis of patients with ESCC. Knock-down of mi R-30 a-3 p/5 p promoted ESCC cell proliferation. Increased mi R-30 a-3 p/5 p expression inhibited the Wnt signaling pathway by targeting Wnt2 and Fzd2.CONCLUSION Down-regulation of mi R-30 a-3 p/5 p promotes ESCC cell proliferation by activating the Wnt signaling pathway through inhibition of Wnt2 and Fzd2.     

ERK信号通路在组胺诱导的大鼠气道平滑肌细胞增殖中的调控作用

目的本研究旨在探讨细胞外信号调节激酶（extracellular signal—regulated kinase,ERK）信号通路在组胺诱导的大鼠气道平滑肌细胞（airway smooth muscle cells,ASMCs）增殖中的调控作用。方法以体外分离、培养的ASMCs为研究对象,加入不同浓度组胺（histanmine,Hist）和PD98059对其进行处理,采用四甲基偶氮唑蓝（MTT）微量比色法检测Hist及ERK信号通路对ASMCs增殖的影响,Western blot检测ERK1／2、磷酸化ERK1／2（phosphorylated-ERK1／2,p-ERK1／2）蛋白的表达,采用酶联免疫吸附试验（ELISA）测定ASMCs核内NF—κB水平,并对各组进行比较。结果低浓度和高浓度的Hist均能不同程度刺激ASMCs增殖,100μmol／L时细胞存活率达201．3％;Hist组ASMCs增殖反应与对照组相比显著增加,而Hist＋PD980059组ASMCs的增殖反应显著低于Hist组;Hist组ASMCs中的p-ERK1／2蛋白表达较正常对照组明显增强,在加入PD980059后Hist诱导的活化ERK1／2相对于Hist组表达显著下降;Hist处理组NF—κB吸光度值显著高于对照组,Hist＋PD98059组NF—κB吸光度值较Hist处理组显著降低。结论Hist可显著诱导ASMCs增殖,ERK信号通道在此调控中起重要作用,而且还可能参与ASMCs中Hist诱导的NF—κB活化。     

Endogenous hydrogen sulfide and ERK1/2 - STAT3 signaling pathway may participate in the association between homocysteine and hypertension

Background Homocysteine (Hcy) is a risk factor for hypertension, although the mechanisms are poorly understood. Methods We first explored the relationship between Hcy levels and blood pressure (BP) by analyzing the clinical data of primary hypertensive patients admitted to our hospital. Secondly, we explored a rat model to study the effect of Hcy on blood pressure and the role of H2S. An hyperhomocysteinemia (HHcy) rat model was induced to explore the effect of Hcy on blood pressure and the possible mechanism. We carried out tissue histology, extraction and examination of RNA and protein. Finally, we conducted cell experiments to determine a likely mechanism through renin-angiotensin-aldosterone system (RAAS) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. Results In primary hypertensive inpatients with HHcy, blood pressure was significantly higher as compared with inpatient counterparts lacking HHcy. In the rat model, blood pressure of the Wistar rats was significantly increased with increases in serum Hcy levels and decreased after folate treatment. Angiotensin converting enzyme 1 (ACE1) expression in the Wistar Hcy group was enhanced comparing to controls, but was decreased in the Wistar folate group. Angiotensin II receptor type 1 (AGTR1) levels in the kidney tissue increased in the Wistar folate group. Both serum H2S and kidney cystathionine γ-lyase decreased with elevated levels of serum Hcy. In vitro, increased concentrations and treatment times for Hcy were associated with increased expression of collagen type 1 and AGTR1. This dose and time dependent response was also observed for p-STAT3 and p-ERK1/2 expression. Conclusion Endogenous H2S might mediate the process of altered blood pressure in response to changes in serum Hcy levels, in a process that is partly dependent on activated RAAS and ERK1/2- STAT3 signaling pathway.     

电针对鱼藤酮诱导的帕金森病模型大鼠黑质内ERK1/2及TNF-α的影响

目的探讨电针对帕金森病(PD)模型大鼠黑质内ERK1/2信号通路及炎症因子肿瘤坏死因子(TNF)-α的作用及机制。方法雄性健康SD大鼠32只,随机分为正常组、假手术组、模型组、电针组,每组8只。模型组和电针组经颈背部注射鱼藤酮造模14 d,造模后进行行为学评价,电针组给予电针"风府"和"太冲"两穴治疗,连续治疗14 d;其余各组不做治疗,假手术组给予相同剂量的DMSO和生理盐水混合液。采用免疫组化法检测大鼠黑质区磷酸化的ERK1/2、酪氨酸羟化酶(TH)、TNF-α阳性细胞表达情况。结果各组大鼠神经行为学表现存在差异,与正常组、假手术组相比,模型组大鼠黑质区TH阳性细胞数减少(P<0.05),磷酸化的ERK1/2、TNF-α阳性细胞数增加(P<0.05);与模型组相比,电针组大鼠黑质区TH阳性细胞数增加(P<0.05),磷酸化的ERK1/2、TNF-α阳性细胞数减少(P<0.05)。结论电针可以通过调节PD模型大鼠体内MAPK/ERK1/2通路,降低p-ERK1/2在PD模型大鼠黑质区的表达,进而减少TNF-α的表达,对PD病的发生发展起到一定的调节作用。     

Hsa_circ_0074491 regulates the malignance of cholesteatoma keratinocytes by modulating the PI3K/Akt pathway by binding to miR-22-3p and miR-125a-5p: An observational study

Cholesteatoma is a benign cystic lesion that can continue to grow like a tumor. Circular ribonucleic acid (RNA) hsa_circ_0074491 (circ_0074491) has been reported to be down-regulated in cholesteatoma tissues. However, the role and regulatory mechanism of circ_0074491 in the growth of cholesteatoma are unclear.The expression of circ_0074491, microRNA (miR)-22-3p, and miR-125a-5p in cholesteatoma tissues was detected by quantitative real-time polymerase chain reaction. The proliferation, cell cycle, apoptosis, migration, and invasion of cholesteatoma keratinocytes were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, plate clone, flow cytometry, or transwell assays. Several protein levels were examined by western blotting. The targeting relationship between miR-22-3p or miR-125a-5p and circ_0074491 was verified via dual-luciferase reporter and RNA pull-down assays.We observed the downregulation of circ_0074491 in cholesteatoma tissues. Furthermore, circ_0074491 knockdown facilitated cell proliferation, migration, invasion, and repressed cell apoptosis in cholesteatoma keratinocytes. Circ_0074491 was verified as a decoy for miR-22-3p and miR-125a-5p in cholesteatoma keratinocytes. Both miR-22-3p and miR-125a-5p silencing reversed the impacts of circ_0074491 silencing on proliferation, apoptosis, migration, and invasion of cholesteatoma keratinocytes. Also, circ_0074491 knockdown activated the PI3K/Akt pathway in cholesteatoma keratinocytes via miR-22-3p and miR-125a-5p.Circ_0074491 played a suppressive role in cholesteatoma through inactivating the PI3K/Akt pathway via binding to miR-22-3p and miR-125a-5p, which provided a novel evidence for the involvement of circRNA in the development of cholesteatoma.     

MicroRNA-30a-5p对肝癌细胞株SMMC-7721增殖凋亡及侵袭转移的影响

目的 探讨转染miRNA-30a-5p对肝癌细胞生物学行为的影响. 方法 将miRNA-30a-5p模拟物、miRNA-30a-5p抑制物瞬时转染入肝细胞肝癌细胞株SMCC-7721,应用实时荧光定量PCR检测正常肝细胞株L02及肝癌细胞株SMCC-7721转染后的miR-30a-5p的mRNA表达情况,CCK-8法检测细胞增殖能力,克隆形成实验检测集落形成情况,流式细胞术检测细胞凋亡及各组细胞周期分布的差异,Transwell小室检测各组细胞体外侵袭转移能力,建立BALB/c-nu裸小鼠肝癌模型并观察miRNA-30a-5p对肿瘤生长的影响. 结果 实时荧光定量PCR显示,与未转染组及正常肝细胞株L02相比,肝癌细胞株SMCC-7721在转染miRNA-30a-5p模拟物后,mRNA表达明显上调(P＜0.01),而转染miRNA-30a-5p抑制物的mRNA表达明显受抑(P＜0.01),差异有统计学意义.肝细胞肝癌细胞株SMCC-7721在转染miRNA-30a-5p模拟物后,细胞活性、克隆形成能力、迁移和侵袭能力与miRNA-30a-5p抑制物转染组、未转染组及正常肝细胞株L02相比,相对减弱(P＜0.05),miRNA-30a-5p模拟物转染组凋亡率,高于miRNA-30a-5p抑制物转染组、未转染组及正常肝细胞株L02 (P＜0.05),细胞周期出现S期阻滞.裸鼠肝癌模型中,实验组裸鼠瘤体质量及体积明显小于空载体对照组和空白对照组(P＜ 0.05).结论 上调miR-30a-5p表达可明显抑制肝细胞肝癌细胞株SMCC-7721的增殖,促进其凋亡,抑制其迁移、侵袭能力,并且抑制裸小鼠肝癌模型肿瘤的生长.     

MiR-197-3p/STAMP2对ox-LDL诱导的人脐静脉内皮细胞凋亡及炎症应激的影响

目的 探究miR-197-3p/前列腺六次跨膜蛋白（Six transmembrane protein of prostate,STAMP）2对氧化型低密度脂蛋白（ox-LDL）诱导的人脐静脉内皮细胞（HUVECs）凋亡和炎症应答。 方法 用ox-LDL处理HUVEC复制内皮细胞损伤模型;RT-PCR检测miR-197-3p和STAMP2表达;ELISA检测细胞凋亡;Western blot用于检测STAMP2,Bax和Bcl-2的蛋白水平;ELISA检测HUVECs中细胞间黏附分子（ICAM）-1,血管内皮细胞黏附分子（VCAM）-1和E选择素（E-selectin）的表达水平;生物信息学预测miR-197-3p的靶基因;并采用双萤光素酶报告系统、qRT-PCR及Western blot验证miR-197-3p与STAMP2的靶向调控关系。 结果 ox-LDL能明显上调miR-197-3p的表达（P<0.05）,同时降低STAMP2的表达（P<0.05）,且呈时间依赖性;下调miR-197-3p能够显著抑制ox-LDL诱导的细胞凋亡（P<0.05）,同时降低促凋亡蛋白Bax并增加抑凋亡蛋白Bcl-2（P<0.05）;抑制miR-197-3p明显降低ox-LDL诱导的炎症因子的表达（P<0.05）;此外,生物信息学预测提示STAMP2是miR-197-3p的靶基因,而且qRT-PCR及Western blot结果显示抑制miR-197-3p明显上调STAMP2 mRNA和蛋白水平（P<0.05）,从而证实miR-197-3p能够靶向调控STAMP2。 结论 MiR-197-3p可以通过靶向调控STAMP2从而调节ox-LDL诱导的HUVECs凋亡及炎症应答,为动脉粥样硬化的靶向治疗提供理论基础。     

过表达miR-140-5p对高脂饲养诱导的非酒精性脂肪性肝病大鼠的作用及机制

目的 探究过表达miR-140-5p对高脂饲养诱导的非酒精性脂肪性肝病(NAFLD)大鼠的作用及机制.方法 40只大鼠随机分为对照组、模型组、空载体组和过表达组,每组各10只.对照组给予普通饲料饲养,模型组给予高脂饲料饲养构建NAFLD大鼠模型,空载体组在模型组基础上于饲养第13周、第18周尾静脉注射含空载质粒的慢病毒...     

高血压性脑出血患者血清miR-141-3p、 miR-29a-3p水平变化及临床意义

目的 观察高血压性脑出血(HICH)患者血清miR-141-3p、miR-29a-3p水平变化,并探讨其与病情以及预后的关系.方法 选择167例HICH患者(HICH组),根据斯堪纳维亚卒中量表(SSS)评分将患者分为轻型组(0～15分,42例)、中型组(16～30分,67例)和重型组(31～45分,58例),根据出院3个月后格拉斯哥预后(GOS)评分分为预后良好组(>4分,87例),预后不良组(≤4分,80例),另选择同期于我院体检的64例健康志愿者(对照组).比较组间血清miR-141-3p、miR-29a-3p和肿瘤坏死因子-α(TNF-α)、IL-1β和IL-6水平.采用Pearson相关分析miR-141-3p、miR-29a-3p与炎性因子的相关性,多因素Logistic回归分析HICH患者预后不良的危险因素,受试者工作特征(ROC)曲线分析miR-141-3p、miR-29a-3p预测HICH患者预后不良的价值.结果 HICH组血清miR-141-3p、miR-29a-3p水平低于对照组,血清TNF-α、IL-1β和IL-6水平高于对照组(P均<0.01).重型组血清miR-141-3p、miR-29a-3p水平低于中型组和轻型组,血清TNF-α、IL-1β、IL-6水平高于中型组和轻型组(P均<0.01);中型组血清miR-141-3p、miR-29a-3p水平低于轻型组,血清TNF-α、IL-1β、IL-6水平高于轻型组(P均<0.01).HICH组血清miR-141-3p、miR-29a-3p水平与TNF-α、IL-1β、IL-6水平均呈负相关(P均<0.01).高水平miR-141-3p(OR=0.656,95％CI:0.500～0.862,P<0.01)、miR-29a-3p(OR=0.733,95％CI:0.581～0.926,P<0.01)是HICH预后的保护因素.miR-141-3p、miR-29a-3p预测HICH预后不良的曲线下面积为0.675、0.688,联合预测曲线下面积为0.898,高于单独指标预测(Z分别为4.950、5.325,P均<0.05).结论 HICH患者血清miR-141-3p、miR-29a-3p水平均降低,且与神经损伤程度加重以及预后不良有关.     

PAX6通过MEK/ERK信号通路抑制肝星状细胞活化和增殖实验研究

目的 探讨PAX6通过丝裂原活化蛋白激酶(MEK)/细胞外调节蛋白激酶(ERK)信号通路抑制肝星状细胞活化和增殖的效果。方法 取LX2肝星状细胞,分为对照组、PAX6 inhibitor组和PAX6 mimics组。采用CCK-8试剂盒测定细胞增殖,采用油红O染色测定细胞分化水平,使用流式细胞仪分析细胞凋亡,采用RT-PCR法和蛋白印迹法测定细胞PAX6、MEK和ERK mRNA和蛋白表达水平。结果 PAX6 inhibitor组细胞PAX6 mRNA水平、凋亡率和G1期分别为(1.49±0.23)、(2.70±0.85)%和(59.02±1.25)%,显著低于LX2肝星状细胞组【分别为(1.85±0.19)、(3.40±0.47)%和(64.66±1.41)%,P<0.05】,而细胞增殖、存活率、分化率、MEK和ERK mRNA和蛋白水平分别为(0.79±0.03)、(73.35±9.74)%、(49.37±4.24)%、(2.55±0.43)、(3.90±0.49)、(0.89±0.15)和(1.17±0.17),显著高于LX2肝星状细胞组【分别为(0.58±0.05)、(6...