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| 1 | Quercetin protects against diabetic retinopathy in rats by inducing heme oxygenase-1 expression显示文摘Quercetin is a widely-occurring flavonoid that protects against cancer, and improves memory and cardiovascular functions.However, whether quercetin exhibits therapeutic effects in diabetic retinopathy remains unclear.In this study, we established a rat model of streptozocininduced diabetic retinopathy.Seventy-two hours later, the rats were intraperitoneally administered 150 mg/kg quercetin for 16 successive weeks.Quercetin markedly increased the thickness of the retinal cell layer, increased the number of ganglion cells, and decreased the overexpression of the pro-inflammatory factors interleukin-1β, interleukin-18, interleukin-6 and tumor necrosis factor-α in the retinal tissue as well as the overexpression of high mobility group box-1 and the overactivation of the NLRP3 inflammasome.Furthermore, quercetin inhibited the overexpression of TLR4 and NF-κBp65, reduced the expression of the pro-angiogenic vascular endothelial growth factor and soluble intercellular adhesion molecule-1, and upregulated the neurotrophins brain-derived neurotrophic factor and nerve growth factor.Intraperitoneal injection of the heme oxygenase-1 inhibitor zinc protoporphyrin blocked the protective effect of quercetin.These findings suggest that quercetin exerts therapeutic effects in diabetic retinopathy possibly by inducing heme oxygenase-1 expression.This study was approved by the Animal Ethics Committee of China Medical University, China(approval No.2016 PS229K) on April 8, 2016. | Guang-Rui Chai Shu Liu Hong-Wei Yang Xiao-Long Chen | 2021 | Neural Regeneration Research2021，16，7： | 15 |
| 2 | 老年糖尿病视网膜病变患者血清中HIF-1α、miR-210水平与微血管损伤的关系显示文摘目的探讨缺氧诱导因子-1α(HIF-1α)、微小RNA-210(miR-210)在老年糖尿病视网膜病变(DR)患者血清中的表达水平及与微血管损伤的关系。方法选取2016年2月至2018年11月诊治的122例DR患者进行研究,称DR组,并以同期收诊的127例单纯糖尿病患者进行对照研究,称单纯糖尿病组;比较两组基本资料;采用实时荧光定量PCR(qRT-PCR)法检测血清HIF-1α、miR-210、血管内皮生长因子(VEGF)表达水平;比较两组外周血内皮细胞(ECs)、内皮祖细胞(EPCs)百分比;比较不同老年DR患者血清HIF-1α、miR-210、VEGF水平及ECs、EPCs含量;分析老年DR患者血清中HIF-1α、miR-210与ECs、EPCs含量的关系及老年DR患者血清中HIF-1α与miR-21的相关性;分析老年DR发生的影响因素。结果DR组收缩压、吸烟史比例、尿微量白蛋白含量、血清HIF-1α、miR-210、VEGF表达水平、外周血ECs含量均明显增高、糖尿病病程长于单纯糖尿病组(P均<0.05),EPCs含量明显低于单纯糖尿病组(P<0.05);DR患者血清中HIF-1α、miR-210表达水平均与ECs含量呈正相关(P均<0.05),与EPCs含量呈负相关(P均<0.05);老年DR患者血清中HIF-1α与miR-21表达水平呈正相关(P<0.05);收缩压、尿微量白蛋白、糖尿病病程、HIF-1α、miR-210、VEGF均是老年DR发生增生型视网膜病变的危险因素(P<0.05)。结论HIF-1α、miR-210在老年DR患者血清中呈高表达,两者与ECs、EPCs含量有关,两者可能影响DR患者微血管损伤的形成,且评估二者水平有助于评估DR发展进程。 | 朱祥祥 陈震 饶卓群 王琼 杨扬 | 2020 | 临床眼科杂志2020，28，4： | 8 |
| 3 | LncRNA-XIST/miR-137/Notch1在糖尿病视网膜病变患者血清和玻璃体中的表达及机制显示文摘目的探讨lncRNA-XIST在糖尿病视网膜病变患者血清和玻璃体中的表达及其机制。方法收集糖尿病视网膜病变患者,同时检测血清和玻璃体中lncRNA-XIST和miR-137的表达量。运用高糖诱导的HRMECs作为体外模型。运用PCR、Western blot、CCK-8、ELISA和荧光素酶报告检查lncRNA-XIST对糖尿病视网膜病变的机制。结果血清和玻璃体中lncRNA-XIST表达量被抑制,miR-137表达量被激活,差异均有统计学意义(P<0.05)。激活lncRNA-XIST能够促进视网膜细胞增殖,减少ROS和MDA的水平,增加GSH、GSH-PX和SOD水平,差异均有统计学意义(P<0.05)。miR-137+lncRNA-XIST减少荧光素酶表达量,miR-137是LncRNA-XIST重要靶点。激活miR-137能够抑制视网膜细胞增殖,提高了ROS和MDA的水平,减少GSH、GSH-PX和SOD水平,差异均有统计学意义。miR-137+Notch1减少荧光素酶表达量,Notch1是miR-137重要靶点。结论lncRNA-XIST/miR-137/Notch1通过ROS及其氧化应激,能够阻止糖尿病视网膜病变,提示lncRNA-XIST可作为预测糖尿病视网膜病变的良好分子标志物。 | 许瑶 娄静 赵峰 | 2020 | 实用医学杂志2020，36，17： | 7 |
| 4 | 长链非编码RNA母系表达基因3调控miR-34a对糖尿病视网膜病变Müller细胞活化及炎症因子分泌的影响显示文摘目的探讨母系表达基因3(maternally expressed gene 3,MEG3)对糖尿病视网膜病变(DR)Müller细胞的活化及炎症因子分泌的影响及机制。方法高脂饮食联合链脲佐菌素腹腔注射构建小鼠DR体内模型。高糖刺激人视网膜Müller细胞株MIO-M1构建DR体外模型。免疫荧光化学染色及Western blot检测小鼠视网膜及Müller细胞中胶质纤维酸性蛋白(GFAP)的表达。Western blot及酶联免疫吸附实验(ELISA)检测小鼠视网膜及细胞培养基上清中血管内皮生长因子(VEGF)蛋白的表达。ELISA检测小鼠视网膜及细胞培养基上清中IL-1β蛋白的表达。分别或同时向Müller细胞中转染pcDNA-MEG3及miR-34a mimic对其表达进行干预。qRT-PCR检测MEG3 mRNA及miR-34a表达。结果与正常对照组小鼠比较,DR组小鼠视网膜中GFAP、VEGF及IL-1β蛋白表达均增多(均为P<0.05),MEG3 mRNA表达降低(P<0.01)。与对照组比较,高糖组Müller细胞中MEG3 mRNA表达降低(P<0.01),而GFAP、VEGF及IL-1β蛋白表达均升高(均为P<0.05)。与高糖组比较,高糖+pcDNA-MEG3组中GFAP、VEGF及IL-1β蛋白表达均降低(均为P<0.05)。与正常对照组比较,DR组小鼠视网膜及高糖刺激的Müller细胞中miR-34a表达均升高(均为P<0.05)。与pcDNA组比较,pcDNA-MEG3组中miR-34a表达减少(P<0.01)。与pcDNA+NC mimic组比较,pcDNA+miR-34a mimic组中GFAP、VEGF及IL-1β蛋白表达均升高(均为P<0.05),而pcDNA-MEG3+NC mimic组中GFAP、VEGF及IL-1β蛋白表达均减少(均为P<0.05)。与pcDNA-MEG3+miR-34a mimic组比较,GFAP、VEGF及IL-1β蛋白表达水平均升高(均为P<0.05)。结论MEG3在DR小鼠视网膜及高糖刺激的Müller细胞中表达均降低,其可通过负向调控miR-34a抑制Müller细胞活化及炎症因子的分泌。过表达MEG3可能成为DR治疗的新靶点。 | 王坤 朱曼辉 陈莉莉 涂园园 万光明 梁申芝 | 2021 | 眼科新进展2021，41，1： | 6 |
| 5 | 微小RNA-126和血管内皮生长因子在增殖性糖尿病视网膜病变患者视网膜前膜中的表达及意义显示文摘目的探讨微小RNA-126(miR-126)和血管内皮生长因子(VEGF)在增殖性糖尿病视网膜病变(PDR)患者视网膜前膜组织中的表达及临床意义。方法选取眼科择期行玻璃体切割手术的PDR患者65例纳入研究组,另选取同期行玻璃体切割手术的特发性黄斑裂孔患者62例纳入对照组。采用实时荧光定量聚合酶链反应(qRT-PCR)法检测2组患者视网膜前膜组织中miR-126、VEGF mRNA表达水平,采用Western blotting法检测VEGF蛋白表达水平,检测患者空腹血糖(FBG)、甘油三酯(TG)、糖化血红蛋白(HbA1c)水平,采用Pearson相关分析法分析miR-126与VEGF mRNA的相关性及两者与FGB、HbA1c、TG的相关性,并对PDR发生的影响因素进行Logistic多元回归分析。结果研究组患者视网膜前膜组织中miR-126表达水平低于对照组,VEGF mRNA及其蛋白表达水平高于对照组,差异有统计学意义(P<0.05);研究组患者FBG、TG和HbA1c水平均高于对照组,差异有统计学意义(P<0.05);miR-126与VEGF mRNA呈显著负相关(P<0.05);miR-126与FGB、HbA1c、TG呈显著负相关(P<0.05),而VEGF mRNA与FGB、HbA1c、TG呈显著正相关(P<0.05);Logistic多元回归分析显示,miR-126与VEGF mRNA表达水平均是患者发生PDR的独立影响因素。结论 PDR患者视网膜前膜组织中miR-126表达显著降低,VEGF表达显著升高,miR-126可能通过负性调控VEGF表达而参与PDR的发生发展。 | 李瑞 李万明 陈小丽 | 2022 | 实用临床医药杂志2022，26，2： | 5 |
| 6 | 丹皮酚对大鼠糖尿病视网膜病变的改善作用及其调节miR-802-5p表达的作用机制显示文摘目的:探讨丹皮酚对大鼠糖尿病视网膜病变(DR)的改善作用,并阐明其可能的作用机制。方法:40只SPF级SD大鼠随机分为对照组、DR模型组、15 mg·kg^(-1)丹皮酚组和30 mg·kg^(-1)丹皮酚组,每组10只,除对照组外其余3组大鼠腹腔注射55 mg·kg^(-1)链脲佐菌素(STZ)构建DR模型。建模成功后,对照组和DR模型组大鼠皮下注射8 mL·kg^(-1)生理盐水,15和30 mg·kg^(-1)丹皮酚组大鼠皮下注射15和30 mg·kg^(-1)丹皮酚磺酸钠注射液,每日1次,共2周。取大鼠视网膜组织用于实时荧光定量PCR(RT-qPCR)、Western blotting和酶联免疫吸附测定(ELISA)检测,HE染色观察各组大鼠视网膜组织病理形态表现。采用高糖(HG,33 mmol·L^(-1)葡萄糖)培养基培养人视网膜微血管内皮细胞(HRMECs)。采用不同剂量(0、5、25、50、70和100 mg·L^(-1))丹皮酚分别干预HRMECs和HG处理24 h后的HRMECs,采用CCK-8法和流式细胞术检测各组细胞活性和凋亡率,以确定后续实验中丹皮酚最适作用剂量。HRMECs进行转染后分为对照组、HG组、HG+NC inhibitor组、HG+miR-802-5p inhibitor组、HG+丹皮酚(25 mg·L^(-1))组、HG+丹皮酚+NC mimic组和HG+丹皮酚+miR-802-5p mimic组。采用RT-qPCR法检测各组大鼠视网膜组织和各组细胞中miR-802-5p表达水平,荧光素酶报告基因和RNA免疫共沉淀法检测HRMECs中miR-802-5p与SIRT6的结合关系,Western blotting法检测各组大鼠视网膜组织和各组细胞中沉默调节蛋白6(SIRT6)、色素上皮衍生因子(PEDF)和血管内皮生长因子(VEGF)蛋白表达水平,ELISA法检测各组大鼠视网膜组织和各组细胞中活性氧(ROS)水平及过氧化氢酶(CAT)和超氧化物歧化酶(SOD)活性。结果:与对照组比较,DR模型组大鼠视网膜组织中miR-802-5p表达水平和VEGF蛋白表达水平明显升高(P<0.01),SIRT6和PEDF蛋白表达水平明显降低(P<0.01),ROS水平明显升高(P<0.01),CAT和SOD活性明显降低(P<0.01);与DR模型组比较,不同剂量丹皮酚组大鼠视网膜组织中miR-802-5p表达水平和VEGF蛋白表达水平明显降低(P<0.05),SIRT6和PEDF蛋白表达水平明显升高(P<0.01),ROS水平明显降低(P<0.05或P<0.01),CAT和SOD活性明显升高(P<0.05或P<0.01)。HE染色,对照组大鼠视网膜组织结构清晰,内外核层细胞排列规则,未见新生血管生成;DR模型组视网膜组织结构不清晰,神经纤维层伴水肿,内外核层细胞排列疏松,有新生血管生成;不同剂量丹皮酚组大鼠视网膜组织结构较DR清晰,内外核层细胞排列较整齐,新生血管生成均较DR模型组有明显改善。与对照组比较,HG组细胞凋亡率升高(P<0.01);与HG组比较,HG+丹皮酚组细胞凋亡率明显降低(P<0.01)。与对照组比较,HG组细胞中miR-802-5p表达水平明显升高(P<0.01);与HG+NC inhibitor组比较,HG+miR-802-5p inhibitor组细胞中miR-802-5p表达水平明显降低(P<0.01)。荧光素酶报告基因分析和RNA免疫共沉淀检测,SIRT6是miR-802-5p的靶基因。与对照组比较,HG组细胞中SIRT6和PEDF蛋白表达水平及CAT和SOD活性明显降低(P<0.01),VEGF蛋白表达水平和ROS水平明显升高(P<0.01);与HG组比较,HG+miR-802-5p inhibitor组细胞中VEGF蛋白表达水平明显降低(P<0.01),SIRT6和PEDF蛋白表达水平明显升高(P<0.01),ROS水平明显降低(P<0.05),CAT和SOD活性明显升高(P<0.01);与HG组比较,HG+丹皮酚组细胞中ROS水平明显降低(P<0.01),CAT和SOD活性明显升高(P<0.01);与HG+丹皮酚+NC mimic组比较,HG+丹皮酚+miR-802-5p mimic组细胞中ROS水平明显升高(P<0.05),CAT和SOD活性明显降低(P<0.01)。结论:丹皮酚可能通过miR-802-5p/SIRT6轴对DR起到一定的改善作用。 | 孙俊波 高达 赵逸菲 许华 邱帆 赵璐 | 2022 | 吉林大学学报(医学版)2022，48，1： | 4 |
| 7 | Transcriptomic analysis reveals essential microRNAs after peripheral nerve injury显示文摘Studies have shown that microRNAs(miRNAs) mediate posttranscriptional regulation of target genes and participate in various physiological and pathological processes, including peripheral nerve injury. However, it is hard to select key miRNAs with essential biological functions among a large number of differentially expressed miRNAs. Previously, we collected injured sciatic nerve stumps at multiple time points after nerve crush injury, examined gene changes at different stages(acute, sub-acute, and post-acute), and obtained mRNA expression profiles. Here, we jointly analyzed mRNAs and miRNAs, and investigated upstream miRNAs of differentially expressed mRNAs using Ingenuity Pathway Analysis bioinformatic software. A total of 31, 42, 30, and 23 upstream miRNAs were identified at 1, 4, 7, and 14 days after rat sciatic nerve injury, respectively. Temporal expression patterns and biological involvement of commonly involved upstream miRNAs(miR-21, let-7, miR-223, miR-10 b, miR-132, miR-15 b, miR-127, miR-29 a, miR-29 b, and miR-9) were then determined at multiple time points. Expression levels of miR-21, miR-132, miR-29 a, and miR-29 b were robustly increased after sciatic nerve injury. Biological processes involving these miRNAs include multicellular organismal response to stress, positive regulation of the epidermal growth factor receptor signaling pathway, negative regulation of epithelial cell differentiation, and regulation of myocardial tissue growth. Moreover, we constructed mechanistic networks of let-7, miR-21, and miR-223, the most significantly involved upstream miRNAs. Our findings reveal that multiple upstream miRNAs(i.e., let-7, miR-21, and miR-223) were associated with gene expression changes in rat sciatic nerve stumps after nerve injury, and these miRNAs play an important role in peripheral nerve regeneration. This study was approved by the Experimental Animal Ethics Committee of Jiangsu Province of China(approval No. 20190303-18) on March 3, 2019. | Yu Wang Shu Wang Jiang-Hong He | 2021 | Neural Regeneration Research2021，16，9： | 4 |
| 8 | miRNA-21对糖尿病肾病诊断效能的Meta分析显示文摘目的 用Meta分析评价miRNA-21作为糖尿病肾病生物学标志物的诊断价值。方法 检索Embase、PubMed、Web of Science、CNKI、万方、VIP、CBM数据库,搜集miRNA-21与糖尿病肾病的相关性研究,检索时间从建库至2021年4月。根据纳入排除标准筛选文献,提取资料,然后采用Revman5.3中的Quadas-2量表进行质量评价,利用Stata15.1以及Meta-Disc1.4软件对纳入研究进行Meta分析并对纳入文献进行偏倚分析及异质性检验。结果 最终纳入7篇文献,共涉及882例样本,其中糖尿病肾病患者525例,对照病例357例。Meta分析结果显示,miRNA-21诊断糖尿病肾病合并敏感度为62%(95%CI:58%~68%),合并特异性为73%(95%CI:68%~78%)。合并阳性似然比为2.50(95%CI:1.79~3.50),合并阴性似然比为0.43(95%CI:0.31~0.60)。合并诊断价值比为6.29(95%CI:3.36~11.79),SROC曲线下AUC面积为0.7889。诊断性试验Deek′s漏斗图显示不存在发表偏倚。研究中有无肾活检可能是异质性一个重要的来源,亚组分析发现miRNA-21在有肾活检报告的研究中有更高的诊断效能(AUC为0.8802)。因此,miRNA-21在糖尿病肾病的诊断效价可能接近肾活检。结论 miRNA-21可作为快速诊断非侵入性糖尿病肾病的新型生物学标志物。 | 钟柯 黄钦 方雅萱 倪清颖 何振洋 杨波 | 2022 | 医学研究杂志2022，51，7： | 3 |
| 9 | MicroRNAs as diagnostic and prognostic biomarkers of age-related macular degeneration:advances and limitations显示文摘A main cause of vision loss in the elderly is age-related macular degeneration(AMD).Among the cellular,biochemical,and molecular changes linked to this disease,inflammation and angiogenesis appear as being crucial in AMD pathogenesis and progression.There are two forms of the disease:dry AMD,accounting for 80–90%of cases,and wet AMD.The disease usually begins as dry AMD associated with retinal pigment epithelium and photoreceptor degeneration,whereas wet AMD is associated with choroidal neovascularization resulting in severe vision impairment.The new vessels are largely malformed,leading to blood and fluid leakage within the disrupted tissue,which provokes inflammation and scar formation and results in retinal damage and detachment.Micro RNAs are dysregulated in AMD and may facilitate the early detection of the disease and monitoring disease progression.Two recent reviews of micro RNAs in AMD had indicated weaknesses or limitations in four earlier investigations.Studies in the last three years have shown considerable progress in overcoming some of these concerns and identifying specific micro RNAs as biomarkers for AMD.Further large-scale studies are warranted using appropriate statistical methods to take into account gender and age disparity in the study populations and confounding factors such as smoking status. | Bridget Martinez Philip V.Peplow | 2021 | Neural Regeneration Research2021，16，3： | 3 |
| 10 | MicroRNAs as biomarkers in glaucoma and potential therapeutic targets显示文摘Glaucoma is a neurodegenerative disease in which optic nerve damage and visual field defects occur.It is a leading cause of irreversible blindness.Its pathogenesis is largely unknown although several risk factors have been identified,with an increase in intraocular pressure being the main one.Lowering of intraocular pressure is the only treatment available.Open-angle glaucoma is the most common form of the condition,accounting for~90%of all cases of glaucoma,with primary open-angle glaucoma and exfoliation glaucoma being the most frequent types.There are strong indications that microRNAs play important roles in the pathogenesis of primary open-angle glaucoma.Most of the recent studies reviewed had performed microRNA profiling in aqueous humor from glaucoma patients compared to controls who were chiefly cataract patients.A very large number of microRNAs were dysregulated but with limited overlap between individual studies.MiRNAs in aqueous humor that could be possible targets for therapeutic intervention are miR-143-3p,miR-125b-5p,and miR-1260b.No ove rlap of findings occurred within the dysregulated miRNAs for blood plasma,blood serum,peripheral blood mononuclear cells,and tears of primary open-angle glaucoma patients.Seve ral impo rtant limitations were identified in these studies.Further studies are warranted of mic roRNA expression in aqueous humor and blood samples of primary open-angle glaucoma patients in the early stages of the disease so that validated biomarkers can be identified and treatment initiated.In addition,whether modifying the levels of specific microRNAs in aqueous humor or tears has a beneficial effect on intraocular pressure and ophthalmic examination of the eyes should be investigated using suitable animal models of glaucoma. | Bridget Martinez Philip V.Peplow | 2022 | Neural Regeneration Research2022，17，11： | 3 |
| 11 | MicroRNAs in laser-induced choroidal neovascularization in mice and rats:their expression and potential therapeutic targets显示文摘Choroidal neovascularization characterizes wet age-related macular degeneration.Choroidal neovascularization formation involves a primarily angiogenic process that is combined with both inflammation and proteolysis.A primary cause of choroidal neovascularization pathogenesis is alterations in pro-and anti-angiogenic factors derived from the retinal pigment epithelium,with vascular endothelium growth factor being mainly responsible for both clinical and experimental choroidal neovascularization.MicroRNAs(miRNAs)which are short,non-coding,endogenous RNA molecules have a major role in regulating various pathological processes,including inflammation and angiogenesis.A review of recent studies with the mouse laser-induced choroidal neovascularization model has shown alterations in miRNA expression in choroidal neovascularization tissues and could be potential therapeutic targets for wet age-related macular degeneration.Upregulation of miR-505(days 1 and 3 post-laser),miR-155(day 14)occurred in retina;miR-342-5p(days 3 and 7),miR-126-3p(day 14)in choroid;miR-23a,miR-24,miR-27a(day 7)in retina/choroid;miR-505(days 1 and 3)in retinal pigment epithelium/choroid;downregulation of miR-155(days 1 and 3),miR-29a,miR-29b,miR-29c(day 5),miR-93(day 14),miR-126(day 14)occurred in retinal pigment epithelium/choroid.Therapies using miRNA mimics or inhibitors were found to decrease choroidal neovascularization lesions.Choroidal neovascularization development was reduced by overexpression of miR-155,miR-188-5p,miR-(5,B,7),miR-126-3p,miR-342-5p,miR-93,miR-126,miR-195a-3p,miR-24,miR-21,miR-31,miR-150,and miR-184,or suppression of miR-505,miR-126-3p,miR-155,and miR-23/27.Further studies are warranted to determine miRNA expression in mouse laser-induced choroidal neovascularization models in order to validate and extend the reported findings.Important experimental variables need to be standardized;these include the strain and age of animals,gender,number and position of laser burns to the eye,laser parameters to induce choroidal neovascularization lesions including wavelength,power,spot size,and duration. | Bridget Martinez Philip V.Peplow | 2021 | Neural Regeneration Research2021，16，4： | 3 |
| 12 | 驻景丸治疗糖尿病视网膜病变网络药理学研究显示文摘采用网络药理学方法探讨驻景丸治疗糖尿病视网膜病变的作用机制.利用TCMSP数据库并结合文献报道,对驻景丸的有效成分进行筛选,通过TCMSP数据库和SymMap数据库,预测有效成分的靶标.通过Disgenet、GeneCards、OMIM数据库搜集糖尿病视网膜病变的相关靶标,并与有效成分作用靶标进行韦恩(Venny)分析,通过比对得到驻景丸治疗糖尿病视网膜病变的关键靶标,采用Cytoscape软件绘制有效成分-关键靶标-疾病可视化网络图.将获得的关键靶标上传至在线STRING数据库进行蛋白质互作分析,并进一步借助Metascape数据库对关键靶标进行GO生物学过程富集分析和KEGG通路富集分析.共获得驻景丸有效成分25个,药物靶标228个,疾病相关基因2889个,药物与疾病共同靶标133个.蛋白互作网络发现AKT1、IL6、TP53、VEGFA、STAT3、MAPK8、TNF、MAPK1、JUN、EGF等可能是驻景丸治疗糖尿病视网膜病变的关键靶标.GO富集分析主要涉及刺激反应、信号通路、生物免疫调节、细胞过程、代谢过程等生物学过程.KEGG富集分析显示驻景丸主要通过调节AGE-RAGE信号通路、癌症信号通路、肿瘤坏死因子信号通路、NF-κB信号通路、胰岛素抵抗等经典信号通路治疗糖尿病视网膜病变.驻景丸治疗糖尿病视网膜病变具有多成分、多靶标、多途径协同作用的特点,为今后驻景丸的作用机制和药物研发提供新思路和参考. | 薛屹 孙向明 胡扬 刘博男 宋辉 凌娜 李文兰 | 2020 | 哈尔滨商业大学学报(自然科学版)2020，36，6： | 2 |
| 13 | miR-28-3p通过PI3K/AKT通路对大鼠糖尿病性视网膜病变及视网膜血管生成的影响显示文摘目的:探讨miR-28-3p通过PI3K/AKT通路对糖尿病性视网膜病变(DR)大鼠及视网膜血管生成的影响。方法:SD大鼠分为假手术组(sham组)、糖尿病模型组(model组)、糖尿病+阴性对照组(miR-NC组)和糖尿病+miR-28-3p inhibitor组(miR-28-3p inhibitor组),采用腹腔注射链脲佐菌素溶液建立糖尿病大鼠模型并给与腺相关病毒(AAV-U6-inhibitor-rno-miR-28-3p-CAG-EGFP)治疗;qPCR检测各组大鼠视网膜组织中miR-28-3p的表达情况;HE染色观察各组大鼠视网膜内血管分布面积情况;免疫荧光检测CD31的表达;免疫组化检测各组大鼠视网膜组织中Bax和Bcl-2蛋白的表达情况;ELISA检测各组大鼠血清中炎性因子(TNF-α、IL-1β和IL-6)的表达情况;Western blotting检测PI3K、AKT蛋白表达情况。结果:与sham组相比,model组大鼠视网膜组织中miR-28-3p的表达上调(P<0.001),与model组相比,miR-28-3p inhibitor组大鼠视网膜组织中miR-28-3p的表达下调(P<0.001);与sham组相比,model组大鼠的视网膜内血管分布面积和CD31的表达明显增加(均P<0.001),与model组相比,miR-28-3p inhibitor组大鼠视网膜血管分布面积和CD31的表达量均降低(均P<0.01);与model组相比,miR-28-3p inhibitor组中Bax的细胞数量降低(P<0.001),Bcl-2的细胞数量增加(P<0.01);与sham组相比,model组大鼠血清中TNF-α、IL-1β和IL-6含量明显增加(均P<0.001),而miR-28-3p inhibitor组大鼠血清中TNF-α、IL-1β和IL-6含量明显降低(均P<0.01);与model组相比,miR-28-3p inhibitor组大鼠视网膜中PI3K和AKT蛋白含量明显下降(均P<0.01)。结论:miR-28-3p inhibitor能抑制视网膜中血管的生成、减轻炎性反应以及抑制凋亡因子Bax表达,促进凋亡抑制因子Bcl-2表达,并且能抑制PI3K/AKT信号通路的激活,在DR发生发展过程有重要作用。 | 闫欢欢 李春花 曾戎 陈红 苏伟 | 2020 | 广西医科大学学报2020，37，8： | 2 |
| 14 | 益气养阴明目方加减对糖尿病视网膜病变患者血糖水平及炎症的影响显示文摘目的探讨益气养阴明目方加减对糖尿病视网膜病变患者血糖水平及炎症的影响。方法选取2019年3月至2020年3月在温岭中医院接受治疗的非增殖期糖尿病视网膜病变患者124例,采用随机数字表法分为对照组、观察组,每组62例,对照组患者使用银杏酮酯滴丸和血明目片进行治疗,观察组在此基础上使用益气养阴明目方治疗,检测两组患者30°内阈值敏感程度、黄斑厚度、出血斑面积、视力水平、视野灰度值;两组糖化血红蛋白(glycosylated hemoglobin,HbA1c)、空腹血糖(fasting plasma glucose,FBG)、餐后2h血糖(2-hour postprandial blood glucose,2hPG)水平;应用酶联免疫吸附法检测C反应蛋白(c-reactionprotein,CRP)水平,并比较两组的临床疗效。结果治疗后,与对照组比较,观察组患者30°内阈值敏感程度较高,黄斑厚度、出血斑面积水平降低(P<0.05)。治疗后,与对照组比较,观察组患者视力水平较高、视野灰度值较低(P<0.05)。治疗后,与对照组比较,观察组患者HbA1c、FBG、2hPG、CRP水平较低(P<0.05)。治疗后,观察组患者治疗总有效率高于对照组(P<0.05)。结论糖尿病视网膜病变患者应用益气养阴明目方加减治疗,可以明显改善患者视力、视野缺损情况,改善患者的血糖水平,并抑制炎症,治疗效果显著,为糖尿病视网膜病变的临床治疗提供参考依据。 | 王天荣 林巧燕 柯赛赛 王荣正 | 2022 | 中国现代医生2022，60，36： | 2 |
| 15 | 577 nm波长激光治疗非增生型糖尿病性视网膜病变的疗效观察显示文摘目的:比较为非增生性视网膜病变(NPDR)患者使用波长为577 nm的激光与波长为532 nm的激光实施全视网膜激光光凝术的效果。方法:选取2018年3月至2020年3月期间右江民族医学院附属医院收治的300例NPDR患者作为研究对象。根据随机数表法将这些患者平均分为长波组和短波组。为长波组患者使用波长为577 nm的激光实施全视网膜激光光凝术,为短波组患者使用波长为532 nm的激光实施全视网膜激光光凝术。然后观察两组患者的玻璃体液中血管内皮生长因子(VEGF)、白细胞介素33(IL-33)及一氧化氮(NO)的水平及最佳矫正视力(BCVA)。结果:治疗后1个月,长波组患者的BCVA高于短波组患者,其玻璃体液中VEGF、IL-33及NO的水平均低于短波组患者,P<0.05。结论:与使用波长为532 nm的激光相比,为NPDR患者使用波长为577 nm的激光实施全视网膜激光光凝术可更有效地提高其视力,降低其玻璃体液中VEGF、IL-33及NO的水平。 | 施智敏 | 2021 | 当代医药论丛2021，19，7： | 1 |
| 16 | 细胞外囊泡miRNA在糖尿病视网膜病变发病机制中的作用显示文摘细胞外囊泡是包含微囊泡、外泌体和凋亡小体的纳米级囊泡,外泌体包含蛋白质、脂质和微小RNA(miRNAs)等内容物。miRNAs是一类高度保守、非编码的小分子RNA,通过与靶基因转录的mRNA互补配对在转录后水平调节靶基因的表达,可在广泛生物细胞分泌的细胞外囊泡中存在。近年来发现miRNAs与糖尿病视网膜病变的发生发展密切相关,是糖尿病视网膜病变的早期检测和治疗的生物标志物。本文就部分miRNAs(miR-126、miR-29b、miR-200b、miR-1273G-3p、miR-93、miR-142-5p)在视网膜的表达以及对其靶基因在糖尿病视网膜病变发病机制中的作用进行综述。 | 陈开传 盛敏杰 李冰 | 2020 | 国际眼科纵览2020，44，2： | 1 |
| 17 | 术前精准评估对局部麻醉下糖尿病视网膜病变患者围术期护理安全的影响显示文摘目的:评价术前精准评估对局麻下糖尿病视网膜病变患者围术期护理安全的影响。方法:选取2018年1月至2018年12月在我院采用局部麻醉方式完成糖尿病视网膜眼底手术的患者68例,随机分为对照组和观察组,各34例。对照组采用传统版手术访视单进行术前评估,观察组使用术前精准护理评估单进行精准评估和访视,制定有针对性的护理计划并施行。比较两组患者的手术满意度及不良事件发生率。结果:干预后,观察组手术满意度高于对照组(P<0.05),不良事件发生率低于对照组(P<0.05)。结论:术前精准评估可降低糖尿病视网膜病变患者不良事件发生率,提高手术满意度,为手术安全提供有益的保障。 | 陈嘉玲 黄杏 王彩萍 钟珊珊 | 2020 | 甘肃医药2020，39，9： | 1 |
| 18 | 芪明颗粒联合复方樟柳碱注射液治疗糖尿病视网膜病变的临床研究显示文摘目的:探究芪明颗粒联合复方樟柳碱注射液治疗糖尿病视网膜病变(diabetic retinopathy,DR)的临床治疗效果。方法:选择2016年9月~2018年5月湖北科技学院附属浠水医院眼科收治的非增殖期糖尿病视网膜病变患者104例作为研究对象,依治疗原则分为对照组52例及治疗组52例,两组均进行常规对症治疗,在此基础上,对照组予以复方樟柳碱注射液治疗,治疗组在对照组基础上联合芪明颗粒治疗,比较研究两组临床疗效、血糖和血脂水平、血液流变学变化及不良反应的发生情况。结果:两组临床总有效率比较,差异具有统计学意义(χ^2=7.792,P=0.005)。治疗后,两组空腹血糖(fasting plasma glucose,FPG)、糖化血红蛋白(hemoglobin A1c,HbA1c)、总胆固醇(total cholesterol,TC)、低密度脂蛋白胆固醇(low density lipoprotein-cholesterol,LDL-C)、全血高切黏度、全血中切黏度、全血低切黏度、血浆黏度、微血管瘤数量及出血灶面积较治疗前明显降低,差异具有统计学意义(P<0.05);且治疗组治后FPG、HbA1c、TC、LDL-C、全血高切黏度、全血中切黏度、全血低切黏度、血浆黏度、微血管瘤数量及出血灶面积明显低于对照组,差异具有统计学意义(P<0.05)。两组不良反应发生率比较,差异无统计学意义(χ^2=0.122,P=0.727)。结论:芪明颗粒联合复方樟柳碱注射液可有效改善非增殖期DR患者临床疗效,其机制可能与改善患者血糖、血脂水平和纠正血液流变学紊乱、减少微血管瘤及出血有关,具有临床推广意义。 | 黄翠 李进 罗文 陈媛媛 | 2021 | 海南医学院学报2021，27，4： | 1 |
| 19 | Inhibition of nitric oxide synthase aggravates brain injury in diabetic rats with traumatic brain injury显示文摘Studies have shown that hyperglycemia aggravates brain damage by affecting vascular endothelial function. However, the precise mechanism remains unclear. Male Sprague-Dawley rat models of diabetes were established by a high-fat diet combined with an intraperitoneal injection of streptozotocin. Rat models of traumatic brain injury were established using the fluid percussion method. Compared with traumatic brain injury rats without diabetic, diabetic rats with traumatic brain injury exhibited more severe brain injury, manifested as increased brain water content and blood-brain barrier permeability, the upregulation of heme oxygenase-1, myeloperoxidase, and Bax, the downregulation of occludin, zona-occludens 1, and Bcl-2 in the penumbra, and reduced modified neurological severity scores. The intraperitoneal injection of a nitric oxide synthase inhibitor N(5)-(1-iminoethyl)-L-ornithine(10 mg/kg) 15 minutes before brain injury aggravated the injury. These findings suggested that nitric oxide synthase plays an important role in the maintenance of cerebral microcirculation, including anti-inflammatory, anti-oxidative stress, and anti-apoptotic activities in diabetic rats with traumatic brain injury. The experimental protocols were approved by the Institutional Animal Care Committee of Harbin Medical University, China(approval No. ky2017-126) on March 6, 2017. | Wan-Chao Yang Hong-Ling Cao Yue-Zhen Wang Ting-Ting Li Hong-Yu Hu Qiang Wan Wen-Zhi Li | 2021 | Neural Regeneration Research2021，16，8： | 1 |
| 20 | MiR-3202对高糖诱导的人视网膜血管内皮细胞损伤的影响显示文摘目的探讨微小RNA-3202(miR-3202)对高糖诱导人视网膜血管内皮细胞(HRCEC)凋亡的影响及其潜在的分子机制。方法体外培养HRCEC,分为低糖组、高糖组、高糖+miR-NC组、高糖+miR-3202组、高糖+si-NC组、高糖+si-ILK组、高糖+miR-3202+pcDNA3.1组和高糖+miR-3202+pcDNA3.1-ILK组。采用实时荧光定量PCR(qRT-PCR)与Western blot法测定HRCEC中miR-3202、整合素连接激酶(ILK)的表达;流式细胞术测定细胞凋亡率;双荧光素酶报告基因实验与Western blot实验验证miR-3202与ILK的靶向调控作用;Western blot测定HRCEC中Bax和Bcl-2蛋白的表达。采用两样本t检验进行统计学分析。结果与低糖组比较,高糖组HRCEC中miR-3202的表达水平(0.95±0.09比0.21±0.02)降低,ILK的表达水平(0.30±0.03比0.86±0.08)、细胞凋亡率(8.54﹪±1.03﹪比28.53﹪±3.25﹪)均升高,差异具有统计学意义(P均<0.05);与高糖+miR-NC组比较,高糖+miR-3202组细胞凋亡率(28.86﹪±2.45﹪比12.67﹪±1.15﹪)、Bax的表达水平(1.12±0.11比0.36±0.03)均下降,Bcl-2的表达水平(0.23±0.02比0.77±0.07)升高,差异具有统计学意义(P均<0.05);与高糖+si-NC组比较,高糖+si-ILK组细胞凋亡率(28.86﹪±2.45﹪比13.46﹪±1.24﹪)、Bax的表达水平(1.10±0.11比0.47±0.05)均降低,Bcl-2的表达水平(0.23±0.02比0.64±0.06)上升,差异具有统计学意义(P均<0.05);miR-3202可负向调控靶基因ILK的表达,ILK过表达可逆转miR-3202对高糖诱导的HRCEC凋亡的作用。结论miR-3202可通过下调ILK的表达而抑制高糖诱导的HRCEC凋亡。 | 罗红 袁昌亮 陈岚 | 2021 | 中华细胞与干细胞杂志(电子版)2021，11，3： | 0 |
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