Article(id=1291404855864709655, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404681641713991, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.07.015, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1728662400000, receivedDateStr=2024-10-12, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824510779, onlineDateStr=2026-08-04, pubDate=1744819200000, pubDateStr=2025-04-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824510779, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824510779, creator=13701087609, updateTime=1785824510779, 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=977, endPage=982, ext={EN=ArticleExt(id=1291404856321888792, articleId=1291404855864709655, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Protective effects of Celosin Ⅰ on rabbit ganglion cells in optic nerve injury model by regulating ROS mediated mitochondrial apoptosis pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the protective mechanism of Celosin Ⅰ on retinal ganglion cells by regulating reactive oxygen species (ROS) mediated mitochondrial apoptosis pathway.
Methods Twenty-four New Zealand white rabbits were randomly divided into sham-operation, model, control and experimental groups, with 6 rabbits per group. The sham-operation group only had the bulbar conjunctiva cut and sutured, the other 3 groups were received with optic nerve clamp injury to contruct the optic nerve injury model. The sham-operation and model groups were given equal volumes of physiological saline by gavage, the control group was given a dose of 0.15 mg·kg-1 mecobalamine solution by gavage, and the experimental group was given a dose of 30 mg·kg-1 Celosin Ⅰ solution by gavage. Four groups were administered a daily gavage treatment for four consecutive weeks. The Tunnel method was used to detect apoptosis of retinal ganglion cells, and immunofluorescence was employed to detect the expression of ROS, superoxide dismutase (SOD) and caspase in retinal tissues. The expression levels of B-cell lymphoma-2 (Bcl-2), Bcl-2-like protein 1 (Bcl-xl), Bcl-2-associated X protein (Bax), and cytochrome C (CytC) proteins in retinal tissues were assessed using Western blotting.
Results After four weeks of intervention, the apoptosis rates of ganglion cells in the experimental, control, model and sham-operated groups were (7.65±1.20)%, (11.65±1.29)%, (17.66±0.93)% and (0.97±0.14)%; the expression levels of ROS in retinal tissues were 6.14±0.57, 8.25±0.96, 16.51±1.07 and 2.05±0.23; the expression levels of SOD were 2.45±0.33, 1.48±0.23, 0.74±0.13 and 3.19±0.30; the expression levels of caspase-3 were 8.55±1.11, 12.68±0.92, 18.74±1.97 and 3.08±0.20; the expression levels of caspase-9 were 3.69±1.20, 7.79±1.13, 12.81±1.72 and 2.31±0.30; the relative expression levels of Bcl-2 were 0.46±0.02, 0.64±0.07, 0.77±0.05 and 0.20±0.03; the relative expression levels of Bcl-xl were 0.46±0.05, 0.61±0.05, 0.78±0.03, and 0.20±0.03; the relative expression levels of Bax were 0.50±0.07, 0.69±0.18, 0.82±0.13 and 0.14±0.04; the relative expression levels of CytC were 0.43±0.15, 0.80±0.14, 1.08±0.19 and 0.26±0.07. The differences in the aforementioned indicators in the experimental group compared with control group were statistically significant (all P<0.05).
Conclusion Celosin Ⅰ reduces ROS levels in retinal tissue of a model of optic nerve injury, inhibits the expression of mitochondrial apoptosis related proteins in retinal ganglion cells, and reduces retinal ganglion cell apoptosis.
, authors=Yi-yan HAN
1, 2, Qu ZHENG
1, 2, 3, Lei ZHAO
4, Bao-qiang DONG
1, 2, Tao ZUO
1, 4, authorsList=Yi-yan HAN, Qu ZHENG, Lei ZHAO, Bao-qiang DONG, Tao ZUO, authorCompany=null, correspAuthors=Tao ZUO, 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=1291404856988783129, articleId=1291404855864709655, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=青葙苷Ⅰ通过调节ROS介导线粒体凋亡途径对视神经损伤模型大白兔节细胞的保护作用, 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 探究青葙苷Ⅰ通过调节活性氧（ROS）介导线粒体凋亡途径对视网膜节细胞保护作用机制。
方法 将24只新西兰大白兔随机分为假手术组、模型组、对照组和实验组，每组6只。假手术组仅切开球结膜并缝合，其他3组用视神经钳夹伤构建视神经损伤模型。假手术组和模型组均给予等体积0.9% NaCl；对照组给予0.15 mg·kg-1甲钴胺溶液；实验组给予剂量30 mg·kg-1青葙苷Ⅰ溶液。4组新西兰大白兔每日灌胃给药1次，连续给药4周。用Tunnel法检测视网膜节细胞的凋亡情况，用免疫荧光法检测视网膜组织中ROS、超氧化物歧化酶（SOD）和胱天蛋白酶（caspase）的表达情况，用蛋白质印迹法检测视网膜组织中B淋巴细胞瘤-2基因（Bcl-2）、Bcl-2样蛋白1（Bcl-xl）、Bcl-2相关X蛋白（Bax）和细胞色素C（CytC）蛋白的表达水平。
结果 干预4周后，实验组、对照组、模型组和假手术组的节细胞凋亡率分别为（7.65±1.20）%、（11.65±1.29）%、（17.66±0.93）%和（0.97±0.14）%，ROS表达水平分别为6.14±0.57、8.25±0.96、16.51±1.07和2.05±0.23，SOD表达水平分别为2.45±0.33、1.48±0.23、0.74±0.13和3.19±0.30，caspase 3表达水平分别为8.55±1.11、12.68±0.92、18.74±1.97和3.08±0.20，caspase 9表达水平分别为3.69±1.20、7.79±1.13、12.81±1.72和2.31±0.30，Bcl-2蛋白相对表达水平分别为0.46±0.02、0.64±0.07、0.77±0.05和0.20±0.03，Bcl-xl蛋白相对表达水平分别为0.46±0.05、0.61±0.05、0.78±0.03和0.20±0.03，Bax蛋白相对表达水平分别为0.50±0.07、0.69±0.18、0.82±0.13和0.14±0.04，CytC蛋白相对表达水平分别为0.43±0.15、0.80±0.14、1.08±0.19和0.26±0.07。实验组的上述指标与对照组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 青葙苷Ⅰ通过降低视神经损伤模型视网膜组织ROS水平，抑制节细胞线粒体凋亡相关蛋白的表达，从而减少视网膜节细胞凋亡。
, authors=韩易言
1, 2, 郑曲
1, 2, 3, 赵磊
4, 董宝强
1, 2, 左韬
1, 4, authorsList=韩易言, 郑曲, 赵磊, 董宝强, 左韬, authorCompany=null, correspAuthors=左韬, authorNote=
韩易言（1993-），女，讲师，主要从事神经损伤修复与再生的相关研究
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韩易言（1993-），女，讲师，主要从事神经损伤修复与再生的相关研究
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2.Key Laboratory of Acupuncture and Moxibustion Health and Rehabilitation, Shenyang 110847, Liaoning Province, China
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1.College of Acupuncture and Moxibustion Massage, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, Liaoning Province, China
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1.辽宁中医药大学 针灸推拿学院，辽宁 沈阳 110847
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