Article(id=1291404805759553757, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404681641713991, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.07.014, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1729094400000, receivedDateStr=2024-10-17, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824498834, onlineDateStr=2026-08-04, pubDate=1744819200000, pubDateStr=2025-04-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824498834, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824498834, creator=13701087609, updateTime=1785824498834, updator=13701087609, issue=Issue{id=1291404681641713991, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='7', pageStart='901', pageEnd='1050', issueExtLink='null', onlineDate='null', pubDate='1744819200000', pubDateStr='2025-04-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824469242, creator='13701087609', updateTime=1785824469242, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=972, endPage=976, ext={EN=ArticleExt(id=1291404805986046174, articleId=1291404805759553757, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Protective effects of etanercept through
miR-30
a on diabetic retinopathy in rats, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To study the effect of etanercept on retinopathy in diabetic rats and explore its mechanism.
Methods Diabetic rat model was established by streptozotocin. The rats were randomly divided into control group (normal feeding), model group (diabetic rat model was established), experimental group (after modeling, etanercept 2 mg·kg-1 was injected subcutaneously into the abdomen twice a week for 12 weeks), and combined group [based on the experimental group, 100 nmol·mL-1 microRNA (miR)-30a inhibitor was injected into the tail vein]. The pathological morphology of retina was observed by hematoxylin-eosin staining. Enzyme-linked immunosorbent assay was used to detect the levels of serum inflammatory factors. The positive expression of glial fibrillary acidic protein (GFAP) in retinal of rats was detected by immunofluorescence staining. The relative expression level of miR-30a in retina was detected by reverse transcription real-time fluorescence quantitative polymerase chain reaction.
Results In the model group, pathological changes occurred in each layer of retina, while in the experimental group, the pathological changes were alleviated, retinal edema was alleviated, cell arrangement was more regular, and the structural boundaries of each layer were clear. In control group, model group and experimental group, the serum levels of interleukin-6 (IL-6) were (0.42±0.07), (1.21±0.16) and (0.69±0.11) μg·L-1, respectively; the levels of IL-1β were (0.26±0.05), (1.82±0.29) and (0.74±0.16) μg·L-1, respectively; the levels of tumour necrosis factor-α(TNF-α) were (0.49±0.08), (1.25±0.17) and (0.72±0.13) μg·L-1, respectively; the relative expression levels of GFAP in retinal tissues were 1.00±0.17, 3.18±0.56 and 1.45±0.23, respectively; the relative expression levels of miR-30a in retinal tissues were 1.00±0.19, 0.61±0.10, and 0.89±0.15, respectively; there were statistical differences between the model group and the control group, and between the experimental group and the model group (all P<0.05).
Conclusion Etanercept can reduce the level of inflammatory factors in diabetic rats, and has a protective effect on diabetic rats retinopathy, its mechanism may be related to the regulation of miR-30a to activate insulin receptor substrate 1/phosphatidylinositol 3 kinase/protein kinase B signaling pathway.
, authors=Nan-jing GUO, Jin LI, Hong-li DENG, authorsList=Nan-jing GUO, Jin LI, Hong-li DENG, authorCompany=null, correspAuthors=Nan-jing GUO, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291404806321590495, articleId=1291404805759553757, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=依那西普通过
miR-30
a对糖尿病大鼠视网膜病变的保护作用, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 研究依那西普对糖尿病大鼠视网膜病变的影响，并探究其机制。
方法 通过链脲佐菌素建立糖尿病大鼠模型。大鼠随机分为对照组（正常饲养）、模型组（建立糖尿病大鼠模型）、实验组（造模后，2 mg·kg-1依那西普腹部皮下注射，每周2次，治疗时间12周）和联合组[基于实验组，尾静脉注射100 nmol·mL-1微小核糖核酸（microRNA，miR）-30a抑制药]。用苏木精-伊红染色法观察大鼠视网膜病理形态，用酶联免疫吸附试验法检测血清炎症因子水平，用免疫荧光染色法检测大鼠视网膜神经胶质纤维酸性蛋白（GFAP）蛋白阳性表达情况，用逆转录实时荧光定量聚合酶链反应检测视网膜中miR-30a相对表达水平。
结果 模型组视网膜的各层结构发生病理变化，实验组视网膜的病理变化有所缓解，视网膜水肿现象减轻，细胞排列较为规则，各层结构界限清晰。对照组、模型组和实验组大鼠血清中白细胞介素-6（IL-6）水平分别为（0.42±0.07）、（1.21±0.16）和（0.69±0.11）μg·L-1，IL-1β水平分别为（0.26±0.05）、（1.82±0.29）和（0.74±0.16）μg·L-1，肿瘤坏死因子-α（TNF-α）水平分别为（0.49±0.08）、（1.25±0.17）和（0.72±0.13）μg·L-1，视网膜组织中GFAP相对表达水平分别为1.00±0.17、3.18±0.56和1.45±0.23，视网膜组织中miR-30a相对表达水平分别为1.00±0.19、0.61±0.10和0.89±0.15，模型组的上述指标与对照组比较，实验组的上述指标与模型组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 依那西普可以降低糖尿病大鼠炎症因子水平，对糖尿病大鼠视网膜病变有保护作用，其机制可能与调控miR-30a激活胰岛素受体底物1/磷脂酰肌醇3激酶/蛋白激酶B信号通路有关。
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