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机构地区:[1]福建医科大学附属第一医院眼科,福州350000
出 处:《临床眼科杂志》2012年第6期552-555,共4页Journal of Clinical Ophthalmology
基 金:福建医科大学学科带头人培养基金课题(No.2007-XKDT)
摘 要:目的通过脂质体介导转染,研究结缔组织生长因子(CTGF)反义寡核苷酸对体外培养人晶状体上皮细胞(HLECs)向纤维组织转分化的影响。方法评估脂质体介导转染对体外培养HLECs的转染率;通过脂质体转染CTGF反义寡核苷酸,测定第3代HLECs细胞生长曲线;采用RT-PCR检测细胞CTGF和α-平滑肌动蛋白(α-SMA)mRNA水平。结果脂质体转染法细胞导入反义核酸阳性率高,脂质体转染24 h后,转化生长因子(TGF-β1)能显著增加CTGF以及α-SMA mRNA的表达,CTGF反义寡核苷酸能抑制这种效应。结论脂质体介导的CTGF反义寡核苷酸转染能有效抑制HLECs TGF-β1诱导的CTGF与α-SMA mRNA表达上调。Objective To investigate the influence of liposomal transfection of CTGF-ASON on transdifferentiafian induced by transforming growth factor-β1 ( TGF-β1 ) in normal human lens epithelium cells ( HLECs ). Methods CTGF- ASON was transduced into normal human lens epithelium cells by α-txansfection with Lipofectamine 2000. The tramfection ratio of FITC-labeled ASON was measured by fluoroscope and the proliferation of HLECs was measured by CCK-8 assay. The expression of CTGF and α-SMA was detected by RT-PCR. Result Lipesomal transfection was high. Culture in TGF- β1 caused profound increase of CTGF and α-SMA that can be inhibited by lipesomal transfection. Condusion Lipesomal transfection of CrGF-ASON can abrogate the influence of TGF-β1 on increase of CTGF and α-SMA mRNA in HLECs.
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