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清肾颗粒对大鼠NRK-52E细胞转分化模型miR-23b和PINK1/Parkin通路的影响 被引量:2
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作者 金华 张叶青 +4 位作者 呼琴 张磊 陈诺 韩燕全 王亿平 《中国药理学通报》 CAS CSCD 北大核心 2024年第1期162-170,共9页
目的 探讨TGF-β1诱导大鼠NRK-52E细胞转分化模型中miR-23b对PINK1/Parkin通路的靶向调节机制,并阐明清肾颗粒含药血清对NRK-52E细胞转分化的干预机理。方法 采用超高效液相色谱(UPLC)指纹图谱法对清肾颗粒进行全指纹图谱分析。构建TGF-... 目的 探讨TGF-β1诱导大鼠NRK-52E细胞转分化模型中miR-23b对PINK1/Parkin通路的靶向调节机制,并阐明清肾颗粒含药血清对NRK-52E细胞转分化的干预机理。方法 采用超高效液相色谱(UPLC)指纹图谱法对清肾颗粒进行全指纹图谱分析。构建TGF-β1诱导大鼠NRK-52E细胞转分化模型,转染siRNA后分为模拟物空载对照组、miR-23b-5p模拟物组、抑制剂空载对照组、miR-23b-5p抑制剂组,观察miR-23b-5p对PINK1表达量的影响。再将NRK-52E细胞分组为正常组、TGF-β1组、清肾颗粒组、miR-23b-mimic-NC组、miR-23b-mimic组、miR-23b-mimic+清肾颗粒组,Western blot法检测NRK-52E细胞中Pink1、Parkin、LC3Ⅱ、Beclin-1、P62、α-SMA蛋白表达,RT-qPCR法检测NRK-52E细胞中miR-23b-5p、Pink1、Parkin、Beclin-1、α-SMA mRNA的表达,双荧光素酶报告基因实验检测miR-23b-5p与PINK1的靶向关系。结果 UPLC指纹图谱法鉴定出清肾颗粒中11个活性成分。miR-23b-5p过表达后,PINK1 mRNA表达量也显著增加(P<0.05);而miR-23b-5p表达沉默后,PINK1 mRNA表达量也显著减少(P<0.05)。双荧光素酶报告显示,Rno-miR-23b-5p能显著下调Rno-PINK1-WT荧光素酶活性(P<0.05),但未能下调突变Rno-PINK1-mut荧光素酶活性(P>0.05)。清肾颗粒含药血清干预实验发现,TGF-β1组的miR-23b-5p、Pink1、Parkin、Beclin-1、LC3Ⅱ表达及LC3Ⅱ/Ⅰ比值均明显低于正常组,P62和α-SMA表达明显高于正常组(P<0.05)。清肾颗粒组和miR-23b-mimic组的miR-23b-5p、Pink1、Parkin、Beclin-1、LC3Ⅱ表达及LC3Ⅱ/Ⅰ比值均明显高于TGF-β1组,P62和α-SMA表达明显低于TGF-β1组(P<0.05)。miR-23b-mimic+清肾颗粒组的表现更优于miR-23b-mimic组(P<0.05)。结论 清肾颗粒能够上调NRK-52E细胞内miR-23b-5p表达,并通过增强PINK1/Parkin通路介导的线粒体自噬活性,抑制NRK-52E细胞转分化进程。 展开更多
关键词 miR-23b-5p pINK1/parkin信号通路 线粒体自噬 NRK-52e细胞 清肾颗粒 上皮细胞转分化
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miR-150-5p靶向ZEB1调控EMT对子宫内膜癌细胞恶性生物学行为的影响 被引量:1
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作者 张桂萍 韩立 彭丽 《实用癌症杂志》 2024年第6期878-882,890,共6页
目的探讨微小RNA-150-5p(miR-150-5p)是否可靶向锌指E盒结合蛋白1(ZEB1)调控子宫内膜癌(EC)细胞上皮间质转化(EMT)进而影响癌细胞的恶性生物学行为。方法RT-qPCR技术检测正常子宫内膜和EC组织中、子宫内膜上皮细胞系hEEC及EC细胞系Ishik... 目的探讨微小RNA-150-5p(miR-150-5p)是否可靶向锌指E盒结合蛋白1(ZEB1)调控子宫内膜癌(EC)细胞上皮间质转化(EMT)进而影响癌细胞的恶性生物学行为。方法RT-qPCR技术检测正常子宫内膜和EC组织中、子宫内膜上皮细胞系hEEC及EC细胞系Ishikawa和HEC-1-A中miR-150-5p相对表达量。过表达miR-150-5p,MTT法、菌落形成实验、伤口愈合实验和Transwell实验分别评估Ishikawa细胞活力、克隆形成、迁移及侵袭能力;双荧光素酶报告基因实验验证miR-150-5p与ZEB1的靶向关系;RT-qPCR检测miR-150-5p及ZEB1 mRNA相对表达量;Western blot技术检测ZEB1、E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)及基质金属蛋白酶9(MMP-9)蛋白表达量。结果与正常子宫内膜组织比较,EC组织中miR-150-5p相对表达量降低(P<0.05);与hEEC细胞比较,HEC-1-A细胞和Ishikawa细胞中miR-150-5p相对表达量降低(P<0.05),Ishikawa细胞中最低(P<0.05)。与空白组比较,miR-150-5p mimics组细胞490 nm处吸光度值、细胞菌落数、迁移数和侵袭数、ZEB1 mRNA和蛋白相对表达量及N-cadherin、Vimentin和MMP-9蛋白相对表达量显著降低,miR-150-5p相对表达量、E-cadherin蛋白相对表达量显著升高(P<0.05)。经生物信息学分析,ZEB1被预测为miR-150-5p的潜在靶基因。结论miR-150-5p可靶向ZEB1抑制癌细胞的恶性生物学行为,其作用机制可能与调控EC细胞EMT进展有关。 展开更多
关键词 微小RNA-150-5p 锌指e盒结合蛋白1 子宫内膜癌 上皮间质转化 恶性生物学行为
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Linc01419调控miR-34a-5p/E2F3轴促进膀胱癌细胞增殖与侵袭
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作者 向威 吕磊 +2 位作者 郑福鑫 袁敬东 吴维 《现代肿瘤医学》 CAS 2024年第16期2921-2929,共9页
目的:探讨长链非编码RNA Linc01419对膀胱癌细胞增殖和侵袭的影响及作用机制。方法:通过UALCAN软件(https://ualcan.path.uab.edu/)分析TCGA数据库中Linc01419在膀胱癌组织与正常膀胱组织中的表达差异;采用实时荧光定量聚合酶链反应(rea... 目的:探讨长链非编码RNA Linc01419对膀胱癌细胞增殖和侵袭的影响及作用机制。方法:通过UALCAN软件(https://ualcan.path.uab.edu/)分析TCGA数据库中Linc01419在膀胱癌组织与正常膀胱组织中的表达差异;采用实时荧光定量聚合酶链反应(real-time fluorescence quantitative polymerase chain reaction,RT-qPCR)检测Linc01419在不同膀胱癌细胞系、22例经病理证实为膀胱癌的手术患者的肿瘤组织及癌旁正常膀胱组织中的表达水平;应用细胞增殖/毒性检测(cell counting kit-8,CCK-8)实验和Transwell小室侵袭实验检测敲低Linc01419表达对膀胱癌细胞增殖与侵袭的影响;采用双荧光素酶报告基因检测法分析Linc01419与miR-34a-5p及miR-34a-5p与E2F3之间的靶向调控关系。结果:UALCAN数据库分析显示相较正常膀胱组织,Linc01419在膀胱癌组织中显著高表达(P<0.001);RT-qPCR分析结果显示相较癌旁正常膀胱组织,Linc01419在22例膀胱癌组织中表达明显上调(P<0.001),与UALCAN数据库分析结果一致;Linc01419在4株膀胱癌细胞中的表达明显高于正常膀胱上皮细胞(P<0.01);敲低Linc01419表达,可显著抑制膀胱癌细胞的增殖、侵袭及N-cadherin、PCNA蛋白的表达,而显著促进E-cadherin的蛋白表达(P<0.05);miR-34a-5p过表达对膀胱癌细胞具有类似的抑制作用;双荧光素酶报告基因实验、RIP及Pull-down实验证实Linc01419可靶向结合miR-34a-5p,而后者进一步介导了对E2F3的靶向调控;抑制miR-34a-5p表达,可显著削弱Linc01419沉默对膀胱癌细胞生物学行为及E-cadherin、N-cadherin、PCNA、E2F3表达的影响。结论:Linc01419在膀胱癌中异常高表达,其通过调控miR-34a-5p/E2F3轴促进膀胱癌细胞增殖和侵袭,很可能是膀胱癌发生、发展过程中的一个重要环节。 展开更多
关键词 膀胱癌 Linc01419 miR-34a-5p e2F3
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p16/Ki-67双染检测、HPVE6/E7mRNA检测在宫颈病变诊断中的价值研究
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作者 彭海兰 梁土玉 +1 位作者 黄之文 李德峰 《黑龙江医药》 CAS 2024年第1期41-44,共4页
目的:探讨p16/Ki-67双染检测、HPVE6/E7mRNA检测在宫颈病变诊断中的价值。方法:选择2021年4月至2023年2月我院收治的605例高危型HPV阳性患者为研究对象,所有患者入院后均进行阴道镜检查与病理活检,取患者细胞学样本分别进行p16/Ki-67双... 目的:探讨p16/Ki-67双染检测、HPVE6/E7mRNA检测在宫颈病变诊断中的价值。方法:选择2021年4月至2023年2月我院收治的605例高危型HPV阳性患者为研究对象,所有患者入院后均进行阴道镜检查与病理活检,取患者细胞学样本分别进行p16/Ki-67双染检测、HPVE6/E7mRNA检测。比较两种方法单独检查与联合检测对宫颈病变阳性检出率的差异;比较三种检查方法对宫颈病变诊断效能的差异。结果:联合检测检出CIN1~3阳性率均高于p16/Ki-67双标记、HPVE6/E7mRNA检测(P<0.05);三种检测方式的浸润癌阳性检出率比较无明显差异(P>0.05)。Kappa检验分析结果显示,p16/Ki-67双标记与HPVE6/E7mRNA检查结果与病理诊断结果具有较好的一致性(Kappa值=0.719,P<0.05);联合检测结果与病理诊断结果具有高度的一致性(Kappa值=0.894,P<0.05)。联合检测对宫颈病变的诊断灵敏度、特异性与准确率高于p16/Ki-67双标记与HPVE6/E7mRNA检查(P<0.05)。结论:p16Ki-67双染与HPVE6/E7mRNA联合检测可准确检出宫颈病变程度,对宫颈病变疾病类型的鉴别可提供充足可靠的数据支持,联合检查的诊断效能较好,对患者后续相关治疗开展有积极指导意义。 展开更多
关键词 p16/Ki-67双标记 HHpVe6/e7mRNA 宫颈病变 鉴别诊断 人乳头瘤病毒
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清胆利肝方治疗肝经郁热型带状疱疹临床疗效及对患者T淋巴细胞亚群、血清疼痛物质P、PGE2的影响 被引量:1
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作者 汪华英 许莹 +1 位作者 郭生红 李彤彤 《中国老年学杂志》 CAS 北大核心 2024年第5期1083-1087,共5页
目的 探讨清胆利肝方治疗肝经郁热型带状疱疹临床疗效及对患者血清疼痛物质(S)P、前列腺素(PG)E2的影响。方法 收集肝经郁热型带状疱疹患者144例,根据随机数字表法随机分为对照组及观察组,每组72例,对照组给予阿昔洛韦及甲钴胺进行常规... 目的 探讨清胆利肝方治疗肝经郁热型带状疱疹临床疗效及对患者血清疼痛物质(S)P、前列腺素(PG)E2的影响。方法 收集肝经郁热型带状疱疹患者144例,根据随机数字表法随机分为对照组及观察组,每组72例,对照组给予阿昔洛韦及甲钴胺进行常规治疗,观察组在对照组用药基础上给予清胆利肝方进行治疗,两组均治疗2 w。对比两组临床疗效,检测治疗前后T淋巴细胞亚群、血清SP、PGE2水平的变化情况,同时记录并比较两组疼痛视觉模拟评分(VAS)及不良反应;治疗后随访2个月,观察后遗神经痛(PHN)的发生情况。结果 治疗后,观察组临床总体有效率显著高于对照组(P<0.05);观察组疱疹结痂消退时间及疼痛缓解时间显著短于对照组(P<0.05)。随访2个月,观察组PHN发生率显著低于对照组(P<0.05)。治疗后,两组血清白细胞介素(IL)-4,IL-6,肿瘤坏死因子(TNF)-α及CD8^(+)水平与治疗前相比明显降低,且观察组上述指标显著低于对照组(P<0.05);治疗后,两组血清CD4^(+)及CD4^(+)/CD8^(+)与治疗前相比显著增加,且观察组升高水平显著高于对照组(P<0.05);治疗后与对照组相比,观察组血清中SP、PGE2显著降低(P<0.05)。结论 清胆利肝方可提高肝经郁热型带状疱疹患者T淋巴细胞亚群水平,降低患者血清中PGE2水平及SP含量,有效减少炎症反应并缓解疼痛。 展开更多
关键词 清胆利肝方 肝经郁热型 带状疱疹 T淋巴细胞亚群 疼痛物质p 前列腺素e2
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长链非编码RNA RP11-497E19.1对胃癌细胞增殖和侵袭的影响及机制实验研究 被引量:1
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作者 伍勇彬 黄山 +1 位作者 姚巧玲 张晓伟 《陕西医学杂志》 CAS 2024年第6期729-733,共5页
目的:探讨长链非编码RNA(lncRNA)RP11-497E19.1对胃癌细胞增殖和侵袭的影响及其机制。方法:实时荧光定量PCR(RT-qPCR)检测胃癌HS-746T、BGC823、NCI-N87、SGC7901、AGS细胞和永生化胃上皮细胞GES-1中RP11-497E19.1表达水平,筛选表达最... 目的:探讨长链非编码RNA(lncRNA)RP11-497E19.1对胃癌细胞增殖和侵袭的影响及其机制。方法:实时荧光定量PCR(RT-qPCR)检测胃癌HS-746T、BGC823、NCI-N87、SGC7901、AGS细胞和永生化胃上皮细胞GES-1中RP11-497E19.1表达水平,筛选表达最高的细胞进行后续实验。将HS-746T细胞分为si-NC组和si-RP11-497E19.1组,分别转染阴性对照寡核苷酸或RP11-497E19.1小干扰RNA。集落形成实验和Transwell实验分析转染HS-746T细胞的增殖、侵袭能力。双荧光素酶报告基因实验验证RP11-497E19.1与微小RNA(miR)-545-5p的靶向关系。RT-qPCR检测转染HS-746T细胞miR-545-5p的表达。Western blot检测转染HS-746T细胞间质表皮转化因子(c-Met)/胆绿素还原酶(BVR)/活化复制因子2(ATF-2)分子通路相关蛋白的表达。结果:与GES-1细胞比较,HS-746T、BGC823、NCI-N87、SGC7901、AGS细胞中RP11-497E19.1表达水平均上升,且HS-746T细胞RP11-497E19.1表达水平最高(均P<0.05)。与si-NC组比较,si-RP11-497E19.1组HS-746T细胞活力和细胞侵袭数降低(均P<0.05)。双荧光素酶报告基因实验证实RP11-497E19.1靶向结合miR-545-5p,可负向调控miR-545-5p表达(P<0.05)。与si-NC组比较,si-RP11-497E19.1组HS-746T细胞c-Met/BVR/ATF-2分子通路蛋白c-Met、BVR、p-ATF-2、锌指蛋白1(Snail1)、锌指蛋白2(Snail2)表达降低(均P<0.05)。结论:胃癌细胞中RP11-497E19.1呈高表达,沉默RP11-497E19.1通过靶向miR-545-5p/c-Met/BVR/ATF-2分子通路抑制胃癌HS-746T细胞的增殖及侵袭。 展开更多
关键词 胃癌 长链非编码RNA Rp11-497e19.1 微小RNA-545-5p 细胞增殖 细胞侵袭 分子通路
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P7C3-A20 treats traumatic brain injury in rats by inhibiting excessive autophagy and apoptosis 被引量:2
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作者 Zhiqing Yang Zhenchao Wang +4 位作者 Xiaoqi Deng Lingxin Zhu Zhaomeng Song Changyu Cao Xinran Li 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第5期1078-1083,共6页
Traumatic brain injury is a severe health problem leading to autophagy and apoptosis in the brain.3,6-Dibromo-beta-fluoro-N-(3-methoxyphenyl)-9H-carbazole-9-propanamine(P7C3-A20)can be neuroprotective in various disea... Traumatic brain injury is a severe health problem leading to autophagy and apoptosis in the brain.3,6-Dibromo-beta-fluoro-N-(3-methoxyphenyl)-9H-carbazole-9-propanamine(P7C3-A20)can be neuroprotective in various diseases,including ischemic stroke and neurodegenerative diseases.However,whether P7C3-A20 has a therapeutic effect on traumatic brain injury and its possible molecular mechanisms are unclear.Therefore,in the present study,we investigated the therapeutic effects of P7C3-A20 on traumatic brain injury and explored the putative underlying molecular mechanisms.We established a traumatic brain injury rat model using a modified weight drop method.P7C3-A20 or vehicle was injected intraperitoneally after traumatic brain injury.Severe neurological deficits were found in rats after traumatic brain injury,with deterioration in balance,walking function,and learning memory.Furthermore,hematoxylin and eosin staining showed significant neuronal cell damage,while terminal deoxynucleotidyl transferase mediated dUTP nick end labeling staining indicated a high rate of apoptosis.The presence of autolysosomes was observed using transmission electron microscope.P7C3-A20 treatment reversed these pathological features.Western blotting showed that P7C3-A20 treatment reduced microtubule-associated protein 1 light chain 3-Ⅱ(LC3-Ⅱ)autophagy protein,apoptosis-related proteins(namely,Bcl-2/adenovirus E1B 19-kDa-interacting protein 3[BNIP3],and Bcl-2 associated x protein[Bax]),and elevated ubiquitin-binding protein p62(p62)autophagy protein expression.Thus,P7C3-A20 can treat traumatic brain injury in rats by inhibiting excessive autophagy and apoptosis. 展开更多
关键词 ApOpTOSIS AUTOpHAGY CORTeX HIppOCAMpUS motor function p7C3-A20 traumatic brain injury
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Dual-targeting AAV9P1-mediated neuronal reprogramming in a mouse model of traumatic brain injury 被引量:1
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作者 Jingzhou Liu Xin Xin +8 位作者 Jiejie Sun Yueyue Fan Xun Zhou Wei Gong Meiyan Yang Zhiping Li Yuli Wang Yang Yang Chunsheng Gao 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第3期629-635,共7页
Traumatic brain injury results in neuronal loss and glial scar formation.Replenishing neurons and eliminating the consequences of glial scar formation are essential for treating traumatic brain injury.Neuronal reprogr... Traumatic brain injury results in neuronal loss and glial scar formation.Replenishing neurons and eliminating the consequences of glial scar formation are essential for treating traumatic brain injury.Neuronal reprogramming is a promising strategy to convert glial scars to neural tissue.However,previous studies have reported inconsistent results.In this study,an AAV9P1 vector incorporating an astrocyte-targeting P1 peptide and glial fibrillary acidic protein promoter was used to achieve dual-targeting of astrocytes and the glial scar while minimizing off-target effects.The results demonstrate that AAV9P1 provides high selectivity of astrocytes and reactive astrocytes.Moreover,neuronal reprogramming was induced by downregulating the polypyrimidine tract-binding protein 1 gene via systemic administration of AAV9P1 in a mouse model of traumatic brain injury.In summary,this approach provides an improved gene delivery vehicle to study neuronal programming and evidence of its applications for traumatic brain injury. 展开更多
关键词 AAV9p1 ASTROCYTeS astrocyte-to-neuron conversion GFAp promoter glial scar induced neurons neuronal reprogramming p1 peptide pTBp1 traumatic brain injury
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Upregulation of circ0000381 atienuates microglial/macrophage pyroptosis after spinal cord injury 被引量:1
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作者 Yan Zhang Wenkai Zhang +4 位作者 Tao Liu Ziqian Ma Wenxiu Zhang Yun Guan Xueming Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第6期1360-1366,共7页
Neuroinflammation exacerbates secondary damage after spinal cord injury,while microglia/macrophage pyroptosis is important to neuroinflammation.Circular RNAs(circRNAs)play a role in the central nervous system.However,... Neuroinflammation exacerbates secondary damage after spinal cord injury,while microglia/macrophage pyroptosis is important to neuroinflammation.Circular RNAs(circRNAs)play a role in the central nervous system.However,the functional role and mechanism of circRNAs in regulating microglia/macrophage pyroptosis after spinal cord injury are still poorly studied.In the present study,we detected microglia/macrophage pyroptosis in a female rat model of spinal cord injury,along with upregulated levels of circ0000381 in the spinal cord.Our further experimental results suggest that circ0000381 may function as a sponge to sequester endogenous microRNA423-3p(miR-423-3p),which can increase the expression of NOD-like receptor 3(NLRP3),a pyroptosis marker.Therefore,upregulation of circ0000381 may be a compensatory change after spinal cord injury to attenuate microglia/macrophage pyroptosis.Indeed,knockdown of circ0000381 expression exacerbated microglia/macrophage pyroptosis.Collectively,our findings provide novel evidence for the upregulation of circ0000381,which may serve as a neuroprotective mechanism to attenuate microglia/macrophage pyroptosis after spinal cord injury.Accordingly,circ0000381 may be a novel therapeutic target for the treatment of spinal cord injury. 展开更多
关键词 circ0000381 INFLAMMASOMe MACROpHAGe microglia miR-423-3p neuroinflammation neuroprotection NLRp3 pYROpTOSIS RNA-Seq spinal cord injury
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Photobiomodulation inhibits the expression of chondroitin sulfate proteoglycans after spinal cord injury via the Sox9 pathway 被引量:1
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作者 Zhihao Zhang Zhiwen Song +12 位作者 Liang Luo Zhijie Zhu Xiaoshuang Zuo Cheng Ju Xuankang Wang Yangguang Ma Tingyu Wu Zhou Yao Jie Zhou Beiyu Chen Tan Ding Zhe Wang Xueyu Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第1期180-189,共10页
Both glial cells and glia scar greatly affect the development of spinal cord injury and have become hot spots in research on spinal cord injury treatment.The cellular deposition of dense extracellular matrix proteins ... Both glial cells and glia scar greatly affect the development of spinal cord injury and have become hot spots in research on spinal cord injury treatment.The cellular deposition of dense extracellular matrix proteins such as chondroitin sulfate proteoglycans inside and around the glial scar is known to affect axonal growth and be a major obstacle to autogenous repair.These proteins are thus candidate targets for spinal cord injury therapy.Our previous studies demonstrated that 810 nm photo biomodulation inhibited the formation of chondroitin sulfate proteoglycans after spinal cord injury and greatly improved motor function in model animals.However,the specific mechanism and potential targets involved remain to be clarified.In this study,to investigate the therapeutic effect of photo biomodulation,we established a mouse model of spinal cord injury by T9 clamping and irradiated the injury site at a power density of 50 mW/cm~2 for 50 minutes once a day for 7 consecutive days.We found that photobiomodulation greatly restored motor function in mice and down regulated chondroitin sulfate proteoglycan expression in the injured spinal cord.Bioinformatics analysis revealed that photobiomodulation inhibited the expression of proteoglycan-related genes induced by spinal cord injury,and versican,a type of proteoglycan,was one of the most markedly changed molecules.Immunofluorescence staining showed that after spinal cord injury,versican was present in astrocytes in spinal cord tissue.The expression of versican in primary astrocytes cultured in vitro increased after inflammation induction,whereas photobiomodulation inhibited the expression of ve rsican.Furthermore,we found that the increased levels of p-Smad3,p-P38 and p-Erk in inflammatory astrocytes were reduced after photobiomodulation treatment and after delivery of inhibitors including FR 180204,(E)-SIS3,and SB 202190.This suggests that Sma d 3/Sox9 and MAP K/Sox9 pathways may be involved in the effects of photobiomodulation.In summary,our findings show that photobiomodulation modulates the expression of chondroitin sulfate proteoglycans,and versican is one of the key target molecules of photo biomodulation.MAPK/Sox9 and Smad3/Sox9 pathways may play a role in the effects of photo biomodulation on chondroitin sulfate proteoglycan accumulation after spinal cord injury. 展开更多
关键词 chondroitin sulfate proteoglycans erk MApK p38 pHOTOBIOMODULATION principal component analysis SMAD3 SOX9 spinal cord injury VeRSICAN
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The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury 被引量:2
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作者 Yijing Zhao Tong Li +6 位作者 Zige Jiang Chengcheng Gai Shuwen Yu Danqing Xin Tingting Li Dexiang Liu Zhen Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第5期1084-1091,共8页
We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation r... We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury. 展开更多
关键词 chemokine(C-X-C motif)ligand 11 cystathionineβsynthase H2S hypoxic ischemic brain injury inflammation L-CYSTeINe lipopolysaccharide microglia miR-9-5p neuroprotection
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Homer1a reduces inflammatory response after retinal ischemia/reperfusion injury 被引量:1
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作者 Yanan Dou Xiaowei Fei +7 位作者 Xin He Yu Huan Jialiang Wei Xiuquan Wu Weihao Lyu Zhou Fei Xia Li Fei Fei 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第7期1608-1617,共10页
Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual damage.Homerla is repo rted to play a protective role in ... Elevated intraocular pressure(IOP)is one of the causes of retinal ischemia/reperfusion injury,which results in NRP3 inflammasome activation and leads to visual damage.Homerla is repo rted to play a protective role in neuroinflammation in the cerebrum.However,the effects of Homerla on NLRP3inflammasomes in retinal ischemia/reperfusion injury caused by elevated IOP remain unknown.In our study,animal models we re constructed using C57BL/6J and Homer1^(flox/-)/Homerla^(+/-)/Nestin-Cre^(+/-)mice with elevated IOP-induced retinal ischemia/repe rfusion injury.For in vitro expe riments,the oxygen-glucose deprivation/repe rfusion injury model was constructed with M uller cells.We found that Homerla ove rexpression amelio rated the decreases in retinal thickness and Muller cell viability after ischemia/reperfusion injury.Furthermore,Homerla knockdown promoted NF-κB P65^(Ser536)activation via caspase-8,NF-κB P65 nuclear translocation,NLRP3 inflammasome formation,and the production and processing of interleukin-1βand inte rleukin-18.The opposite results we re observed with Homerla ove rexpression.Finally,the combined administration of Homerla protein and JSH-23 significantly inhibited the reduction in retinal thickness in Homer1^(flox/-)Homer1a^(+/-)/Nestin-Cre^(+/-)mice and apoptosis in M uller cells after ischemia/reperfusion injury.Taken together,these studies demonstrate that Homer1a exerts protective effects on retinal tissue and M uller cells via the caspase-8/NF-KB P65/NLRP3 pathway after I/R injury. 展开更多
关键词 CASpASe-8 Homer1a INTeRLeUKIN-18 INTeRLeUKIN-1Β intraocular pressure ischemia/reperfusion injury JSH-23 Müller cells NLRp3 nuclear factor-kB p65 ReTINA
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血清KYNA、EP4在老年急性心肌梗死患者中表达水平及其与心肌损伤预后的相关性
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作者 刘军 彭娟娥 +3 位作者 黄婷 黄倩 刘漓勇 蔡烈松 《成都医学院学报》 CAS 2024年第5期832-835,840,共5页
目的探讨老年急性心肌梗死(AMI)患者血清犬尿喹啉酸(KYNA)、E-前列腺素受体4(EP4)表达与心肌损伤预后的相关性。方法选取长江大学附属仙桃市第一人民医院收治的87例老年AMI患者作为试验组,同时选择80例老年健康体检者作为对照组,试验组... 目的探讨老年急性心肌梗死(AMI)患者血清犬尿喹啉酸(KYNA)、E-前列腺素受体4(EP4)表达与心肌损伤预后的相关性。方法选取长江大学附属仙桃市第一人民医院收治的87例老年AMI患者作为试验组,同时选择80例老年健康体检者作为对照组,试验组依据预后情况分为预后良好组(75例)及预后不良组(12例)。检测血清KYNA、EP4及心肌酶指标cTnI、CK-MB、CK表达水平;血清KYNA、EP4与心肌酶指标的相关性采用Pearson相关性分析;KYNA、EP4水平与老年AMI患者预后的关系采用Kaplan-Meier生存曲线分析;老年AMI患者预后不良的影响因素采用多因素COX回归分析。结果试验组TG、LDL-C及TC高于对照组(P<0.05),试验组患者血清KYNA及心肌酶指标cTnI、CK-MB及CK的表达水平升高,EP4表达水平降低(P<0.05);相关性分析显示,血清KYNA与心肌酶指标呈正相关,EP4与心肌酶指标呈负相关;血清KYNA低表达患者3年生存率高于高表达患者,EP4高表达患者3年生存率高于低表达患者。预后不良组cTnI、CK-MB、CK及KYNA水平高于预后良好组,EP4水平低于预后良好组(P<0.05),KYNA、EP4是AMI预后不良的影响因素(P<0.05)。结论老年AMI患者血清KYNA表达水平升高,血清EP4表达水平降低,二者与患者心肌损伤的预后相关。 展开更多
关键词 老年急性心肌梗死 犬尿喹啉酸 e-前列腺素受体4 心肌损伤 预后
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MiRNA-145-5p inhibits gastric cancer progression via the serpin family E member 1-extracellular signal-regulated kinase-1/2 axis 被引量:1
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作者 Hong-Xia Bai Xue-Mei Qiu +1 位作者 Chun-Hong Xu Jian-Qiang Guo 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第5期2123-2140,共18页
BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC... BACKGROUND MicroRNAs(miRNAs)regulate gene expression and play a critical role in cancer physiology.However,there is still a limited understanding of the function and regulatory mechanism of miRNAs in gastric cancer(GC).AIM To investigate the role and molecular mechanism of miRNA-145-5p(miR145-5p)in the progression of GC.METHODS Real-time polymerase chain reaction(RT-PCR)was used to detect miRNA expression in human GC tissues and cells.The ability of cancer cells to migrate and invade was assessed using wound-healing and transwell assays,respectively.Cell proliferation was measured using cell counting kit-8 and colony formation assays,and apoptosis was evaluated using flow cytometry.Expression of the epithelial-mesenchymal transition(EMT)-associated protein was determined by Western blot.Targets of miR-145-5p were predicated using bioinformatics analysis and verified using a dual-luciferase reporter system.Serpin family E member 1(SERPINE1)expression in GC tissues and cells was evaluated using RT-PCR and immunohistochemical staining.The correlation between SERPINE1 expression and overall patient survival was determined using Kaplan-Meier plot analysis.The association between SERPINE1 and GC progression was also tested.A rescue experiment of SERPINE1 overexpression was conducted to verify the relationship between this protein and miR-145-5p.The mechanism by which miR-145-5p influences GC progression was further explored by assessing tumor formation in nude mice.RESULTS GC tissues and cells had reduced miR-145-5p expression and SERPINE1 was identified as a direct target of this miRNA.Overexpression of miR-145-5p was associated with decreased GC cell proliferation,invasion,migration,and EMT,and these effects were reversed by forcing SERPINE1 expression.Kaplan-Meier plot analysis revealed that patients with higher SERPINE1 expression had a shorter survival rate than those with lower SERPINE1 expression.Nude mouse tumorigenesis experiments confirmed that miR-145-5p targets SERPINE1 to regulate extracellular signal-regulated kinase-1/2(ERK1/2).CONCLUSION This study found that miR-145-5p inhibits tumor progression and is expressed in lower amounts in patients with GC.MiR-145-5p was found to affect GC cell proliferation,migration,and invasion by negatively regulating SERPINE1 levels and controlling the ERK1/2 pathway. 展开更多
关键词 Gastric cancer MicroRNA-145-5p Serpin family e member 1 epithelial-mesenchymal transition proliferation extracellular signal-regulated kinase-1/2
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Exercise-induced modulation of miR-149-5p and MMP9 in LPS-triggered diabetic myoblast ER stress: licorice glycoside E as a potential therapeutic target 被引量:1
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作者 Yi Du Hong Liu 《Traditional Medicine Research》 2024年第8期23-34,共12页
Background:This study explores the relationship between endoplasmic reticulum(ER)stress and diabetes,particularly focusing on the impact of physical exercise on ER stress mechanisms and identifying potential therapeut... Background:This study explores the relationship between endoplasmic reticulum(ER)stress and diabetes,particularly focusing on the impact of physical exercise on ER stress mechanisms and identifying potential therapeutic drugs and targets for diabetes-related sepsis.The research also incorporates traditional physical therapy perspectives,emphasizing the genomic insights gained from exercise therapy in disease management and prevention.Methods:Gene analysis was conducted on the GSE168796 and GSE94717 datasets to identify ER stress-related genes.Gene interactions and immune cell correlations were mapped using GeneCard and STRING databases.A screening of 2,456 compounds from the TCMSP database was performed to identify potential therapeutic agents,with a focus on their docking potential.Techniques such as luciferase reporter gene assay and RNA interference were used to examine the interactions between microRNA-149-5p and MMP9.Results:The study identified 2,006 differentially expressed genes and 616 miRNAs.Key genes like MMP9,TNF-α,and IL1B were linked to an immunosuppressive state.Licorice glycoside E demonstrated high affinity for MMP9,suggesting its potential effectiveness in treating diabetes.The constructed miRNA network highlighted the regulatory roles of MMP9,IL1B,IFNG,and TNF-α.Experimental evidence confirmed the binding of microRNA-149-5p to MMP9,impacting apoptosis in diabetic cells.Conclusion:The findings highlight the regulatory role of microRNA-149-5p in managing MMP9,a crucial gene in diabetes pathophysiology.Licorice glycoside E emerges as a promising treatment option for diabetes,especially targeting MMP9 affected by ER stress.The study also underscores the significance of physical exercise in modulating ER stress pathways in diabetes management,bridging traditional physical therapy and modern scientific understanding.Our study has limitations.It focuses on the microRNA-149-5p-MMP9 network in sepsis,using cell-based methods without animal or clinical trials.Despite strong in vitro findings,in vivo studies are needed to confirm licorice glycoside E’s therapeutic potential and understand the microRNA-149-5p-MMP9 dynamics in real conditions. 展开更多
关键词 eR stress diabetes physical exercise gene expression microRNA-149-5p MMp9 licorice glycoside e traditional physical therapy genomics insights
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miR-30a-5p靶向E2F7阻滞A549细胞周期并抑制其增殖
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作者 鲍祯 乔亚红 《河南医学研究》 CAS 2024年第17期3106-3113,共8页
目的探究miR-30a-5p靶向E2F7调控非小细胞肺癌细胞周期和增殖的机制。方法通过荧光定量(qRT-PCR)验证miR-30a-5p在非小细胞肺癌A549细胞与人正常肺上皮细胞BEAS-2B中的相对表达水平。在线软件预测了miR-30a-5p的靶基因及其靶向结合位点... 目的探究miR-30a-5p靶向E2F7调控非小细胞肺癌细胞周期和增殖的机制。方法通过荧光定量(qRT-PCR)验证miR-30a-5p在非小细胞肺癌A549细胞与人正常肺上皮细胞BEAS-2B中的相对表达水平。在线软件预测了miR-30a-5p的靶基因及其靶向结合位点,双荧光素酶报告基因实验进一步验证miR-30a-5p和E2F7 mRNA 3’UTR区域的靶向关系。其次在A549细胞中分别转染miR-30a-5p模拟物(miR-30a-5p mimics)和miR-30a-5p抑制剂(miR-30a-5p inhibitor),应用CCK-8细胞计数试剂盒检测A549细胞增殖情况,流式细胞术检测A549细胞凋亡和细胞周期。qRT-PCR和免疫印迹检测细胞周期相关基因和肺腺癌相关基因的mRNA和蛋白表达水平。结果miR-30a-5p在A549细胞中表达水平低于BEAS-2B,且miR-30a-5p靶向结合与E2F7 mRNA 3’UTR 514-520位点,抑制E2F7表达。转染miR-30a-5p mimics抑制A549细胞增殖,并促进A549凋亡。将A549细胞周期阻滞在G 1期。调控肺腺癌相关基因TFDP3、CDK1、E2F8、CCNA2和CDC6的mRNA和蛋白表达水平。结论非小细胞肺癌A549细胞中miR-30a-5p通过靶向负调控E2F7的表达,调控TFDP3、CDK1、E2F8、CCNA2和CDC6的mRNA和蛋白表达,抑制A549细胞增殖和细胞周期。 展开更多
关键词 非小细胞肺癌 miR-30a-5p e2F7 基因表达 细胞周期 凋亡
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急性心肌梗死患者外周血内皮细胞微粒中miR-126和P-选择素及E-选择素水平特点及其临床意义
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作者 马清玉 马艺萍 +4 位作者 阿卜拉江·艾合麦提 尼格热·阿力木 帕丽达·玉山江 刘柯 穆叶赛·尼加提 《中国心血管病研究》 CAS 2024年第7期600-605,共6页
目的分析急性心肌梗死(AMI)患者外周血内皮细胞微粒(EMPs)中miR-126、P-选择素、E-选择素的表达水平,探究其与AMI的关系及临床意义。方法选择2021年9月至2022年9月新疆维吾尔自治区人民医院收治的45例AMI患者作为研究组,45例同期健康体... 目的分析急性心肌梗死(AMI)患者外周血内皮细胞微粒(EMPs)中miR-126、P-选择素、E-选择素的表达水平,探究其与AMI的关系及临床意义。方法选择2021年9月至2022年9月新疆维吾尔自治区人民医院收治的45例AMI患者作为研究组,45例同期健康体检者作为对照组。冠状动脉狭窄的评估基于冠状动脉病变数量和Genisi评分。利用流式细胞仪检测外周血中的EMPs,用PCR法检测EMPs中的miR-126表达水平,通过ELISA法测定EMPs中的P-选择素、E-选择素表达。结果AMI组外周血EMPs中miR-126水平低于健康组,P-选择素和E-选择素水平显著高于健康组。外周血EMPs中miR-126水平在三支血管病变组中的表达水平明显低于双支病变组和单支病变组,且外周血EMPs中miR-126水平与Genisi评分呈负相关。外周血EMPs中P-选择素水平在三支血管病变组中的表达水平明显高于双支病变组和单支病变组,且P-选择素与Genisi评分呈正相关。多因素logistic回归显示,外周血EMPs中P-选择素、E-选择是AMI的危险因素。受试者工作曲线(ROC)分析结果显示,外周血EMPs中miR-126、P-选择素及E-选择素单独诊断AMI的效能较低,外周血EMPs中miR-126、P-选择素及E-选择素联合诊断AMI具有良好的诊断效能。结论外周血EMPs中P-选择素和E-选择素是AMI的危险因素。外周血EMPs中miR-126、P-选择素及E-选择素联合对AMI有诊断价值,可作为AMI诊断的生物学标志物。 展开更多
关键词 急性心肌梗死 内皮细胞微粒 MIR-126 p-选择素 e-选择素
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Field Assessment of the Level of Protection Conferred by a Newly Prepared Combined Inactivated Vaccine against E. coli and P. multocida in Rabbit in Egypt
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作者 Eman M. El Rawy Wafaa S. Abd El-Moneim +5 位作者 Fatma M. Gad Fatma F. Ibrahim Fatma El Zahraa Gamal Abeer Mwafy Manar F. Seioudy Selim S. Salama 《World Journal of Vaccines》 CAS 2024年第2期43-56,共14页
Pasteurellosis is the most prevalent, extremely contagious bacterial disease among domestic rabbits and is considered the leading cause of deaths in rabbits, resulting in enormous economic losses to the rabbit industr... Pasteurellosis is the most prevalent, extremely contagious bacterial disease among domestic rabbits and is considered the leading cause of deaths in rabbits, resulting in enormous economic losses to the rabbit industry. Screening for bacterial agents causing mortalities in rabbits revealed the presence of Enterobacteriacae species in approximately 42% of studied cases, with E. coli the most commonly isolated organism. The present study was designed to evaluate the immune response of rabbits vaccinated with a locally prepared, combined inactivated vaccine of Pasteurella multocida and E. coli, adjuvanated with Montanide ISA70. A total of 370 rabbits, aged 2 - 3 weeks, were divided into four groups: (G1) vaccinated with a polyvalent P. multocida vaccine, (G2) vaccinated with a polyvalent E. coli vaccine, (G3) vaccinated with a combined inactivated Montanide ISA70 vaccine of P. multocida and E. coli, and (G4) kept as a non-vaccinated control group. All rabbits received two doses of 0.5 ml of the prepared vaccines, administered one month apart, and were then challenged with virulent strains of P. multocida and E. coli three weeks after the second vaccination. The prepared vaccines were evaluated by determining humoral immunity using indirect haemagglutination (IHA) test and ELISA. The potency of the vaccines was assessed through challenge and determination of LD50. Experimental findings on the prepared polyvalent combined inactivated P. multocida and E. coli vaccine indicated that it is a potent vaccine, producing the highest antibody titers and a 90% protection rate against challenges with virulent strains of P. multocida type A, D2, and E. coli types O157, O151 and O125. Thus, this vaccine is promising in addressing both P. multocida and E. coli problems in rabbits, farms, providing significant protection, and we recommend its commercial production to help rabbit producers control these two major bacterial infections. 展开更多
关键词 p. multocida e. coli Vaccine eLISA Challenge Test Rabbit protection
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CK34βE12、P504s、Ki-67在前列腺癌的表达及其临床意义分析
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作者 王磊 薛永豪 +2 位作者 刘星达 刘鸿宇 王超奇 《内蒙古民族大学学报(自然科学版)》 2024年第5期43-47,共5页
研究收集95例前列腺癌(PCa)和良性前列腺增生(BPH)患者的样本,采用免疫组化技术检测CK34βE12、P504s、Ki-67的表达情况,旨在分析CK34βE12、P504s、Ki-67在前列腺癌中的表达情况及其临床意义。结果显示:与BPH样本相比,PCa样本中P504s和... 研究收集95例前列腺癌(PCa)和良性前列腺增生(BPH)患者的样本,采用免疫组化技术检测CK34βE12、P504s、Ki-67的表达情况,旨在分析CK34βE12、P504s、Ki-67在前列腺癌中的表达情况及其临床意义。结果显示:与BPH样本相比,PCa样本中P504s和Ki-67的阳性率显著升高,而CK34βE12的阳性率则显著降低。此外,P504s和Ki-67的表达与前列腺癌的病理分期和Gleason评分均相关。因此,本研究认为CK34βE12、P504s、Ki-67联合检测在前列腺癌的诊断及肿瘤进展评估中具有较高价值。 展开更多
关键词 前列腺癌 CK34Βe12 p504S KI-67 临床意义
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Preliminary study on the protective effect of electroacupuncture Neiguan acupoint pretreatment on rats with myocardial ischemia-reperfusion injury:role of the miR-214-3p/NCX1 axis
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作者 Hai-Long Fan Ya-Qin Liu +4 位作者 Li-Li Jiang Qi-Rong Li Li-Li Niu Li-Zhen Yang Fu-Ran Du 《Integrative Medicine Discovery》 2024年第27期1-11,共11页
Background:Ischemia-reperfusion can worsen myocardial damage and increase the risk of death.Studies have revealed that ischemic preconditioning provides the best endogenous protection against myocardial ischemia-reper... Background:Ischemia-reperfusion can worsen myocardial damage and increase the risk of death.Studies have revealed that ischemic preconditioning provides the best endogenous protection against myocardial ischemia-reperfusion injury(MIRI),and the principle of electroacupuncture(EA)preconditioning is comparable to that of myocardial ischemic preconditioning adaption.Our earlier research demonstrated that EA pretreatment inhibits the expression of calmodulin-dependent protein kinase IIδ(CaMKIIδ),sodium/calcium exchanger 1(NCX1),and cyclophilin D,hence providing protection against MIRI.However,the exact mechanism is still unknown.The expression of NCX1 mRNA is directly regulated by microRNA-214(miR-214).Moreover,it suppresses the levels of CaMKIIδand cyclophilin D.Whether these variables contribute to EA preconditioning to improve MIRI needs to be investigated,though.This study aimed to preliminarily determine whether EA pretreatment ameliorates MIRI by modulating the miR-214-3p/NCX1 axis.Methods:We used a rat MIRI model to investigate the effect of EA pretreatment on MIRI and the expression of miR-214-3p.In addition,adenovirus injection inhibited miR-214-3p expression in the rat MIRI model,and the influence of EA pretreatment towards MIRI was observed in the context of blocked miR-214-3p expression.Both the myocardial histological abnormalities and the alterations in the ST segment of the rat electrocardiogram were analyzed.NCX1 mRNA,cyclophilin D,and CaMKIIδexpression levels were also analyzed.Results:EA pretreatment improved MIRI.In rats with MIRI,EA administration increased miR-214-3p expression while decreasing NCX1 mRNA,cyclophilin D,and CaMKIIδproteins in cardiac tissues.The beneficial effect of EA pretreatment against MIRI was reversed,coupled with elevated levels of NCX1 mRNA,cyclophilin D,and CaMKIIδprotein expression,when an adenovirus injection disrupted the expression of miR-214-3p.Conclusions:Our findings preliminarily show that EA pretreatment inhibits the expression of NCX1 mRNA,cyclophilin D,and CaMKIIδproteins via miR-214-3p,hence exerting MIRI protection. 展开更多
关键词 myocardial ischemia-reperfusion injury miR-214-3p NCX1 eLeCTROACUpUNCTURe protective effect
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