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作 者:彭佳媛 杜旌畅 钟茜 刘婷婷 杨利琼 吴蔼林 陈玮 朱彦锋 余小平 Jia-Yuan Peng;Jing-Chang Du;Qian Zhong;Ting-Ting Liu;Li-Qiong Yang;Ai-Lin Wu;Wei Chen;Yan-Feng Zhu;Xiao-Ping Yu(Department of Public Health,Chengdu Medical College,Chengdu 610500,Sichuan Province,China)
机构地区:[1]成都医学院公共卫生学院
出 处:《国际眼科杂志》2019年第10期1657-1662,共6页International Eye Science
基 金:国家自然科学基金资助项目(No.81773432,81573154)~~
摘 要:目的:探讨飞燕草素(Dp)防护光诱导的视网膜氧化应激损伤的机制。方法:将661W感光细胞经2 000Lx光照(48h)和/或不同浓度Dp(5、10、20μmol/L,24h)处理,分别测定细胞活性和乳酸脱氢酶(LDH)活力、硫代巴比妥酸活性物质(TBARS)含量及抗氧化酶系[超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽巯基转移酶(GST)]活性。将健康SD大鼠经3 000Lx光照(24h)和/或Dp[100mg/(kg·d),灌胃4wk]处理后,观察视网膜的组织结构和氧化应激指标(SOD、GSH-Px、GST)变化。结果:细胞实验结果表明,光照后细胞活性显著降低,细胞LDH活力和TBARS含量升高,抗氧化酶系活性下降,而Dp处理能提高光照后细胞的活力,降低细胞LDH活力和TBARS含量,提高抗氧化酶系活性。动物实验结果表明,Dp可保护大鼠视网膜结构的完整性,降低视网膜组织中TBARS含量,升高SOD、GSH-Px、GST活性。结论:Dp可能通过调控氧化-抗氧化系统有效防护光化学因素导致的视网膜损伤。AIM:To investigate the mechanism of Delphinidin(Dp)in protecting retinal against light induced oxidative damage.METHODS:All 661W photosensitive cells were treated with 2 000Lx light(48h)and/or different concentrations of Dp(5,10,20μmol/L,24h).Cell activity,intracellular LDH activity,TBARS content and antioxidant enzymes(SOD,GSH-Px,GST)activity were determined respectively.After the healthy SD rats were treated with 3 000 Lx light(24h)and/or Dp[100mg/(kg·d)for 4wk],then changes in retinal tissue structure were observed and fluctuations in oxidative stress index(SOD,GSH-Px,GST)were determined.RESULTS:The results of in vitro experiments showed that the cell activity was significantly decreased after irradiation,the LDH activity and TBARS content were increased,and the activity of antioxidant enzyme system were decreased.However,Dp treatment could increase cell viability,decrease LDH activity and TBARS content,and increase the activity of antioxidant enzyme system.In vivo experiments showed that Dp can protect the structural integrity of retina,reduce the content of TBARS in retinal tissue,and increase the activity of SOD,GSH-Px and GST.CONCLUSION:Dp may protect retinal against Photochemical factors-induced oxidative damage by regulating the oxidation-antioxidant system.
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