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作 者:王艳 刘畅[1,2,3] 靳二辉 赵磊[1,2,3] 胡倩倩 路振香[1,2,3] 李磊 WANG Yan;LIU Chang;JIN Erhui;ZHAO Lei;HU Qianqian;LU Zhenxiang;LI Lei(College of Animal Science,Anhui Science and Technology University,Fengyang 233100,China;Key Laboratory of Quality&Safety Control for Pork,Ministry of Agriculture and Rural Affairs,Fengyang 233100,China;Anhui Province Key Laboratory of Animal Nutritional Regulation and Health,Fengyang 233100,China)
机构地区:[1]安徽科技学院动物科学学院,安徽凤阳233100 [2]农业农村部猪肉质量安全控制重点实验室,安徽凤阳233100 [3]动物营养调控与健康安徽省重点实验室,安徽凤阳233100
出 处:《安徽科技学院学报》2022年第1期7-12,共6页Journal of Anhui Science and Technology University
基 金:安徽省自然科学基金(2008085QC146);安徽省高校优秀青年骨干人才国外访问研修项目(gxgwfx2019047);安徽科技学院人才引进项目(ZRC2014447);安徽省重点研究与开发计划项目(202004a06020050);安徽省高校优秀人才支持计划项目(gxyq2021199)。
摘 要:目的:观察镉对小鼠肝细胞氧化损伤作用,为研究镉的肝毒性作用机制提供基础。方法:首先,采用Cell Counting Kit-8(CCK-8)试剂盒检测镉对小鼠肝细胞活力的影响,然后通过苏木精-伊红染色(Hematoxylin-eosin staining,HE)和Hoechst 33342染色观察细胞病理变化情况,最后通过测定细胞超氧化物歧化酶(Superoxide dismutase,SOD)、丙二醛(Malondialdehyde,MDA)的含量,评价镉诱导小鼠肝细胞氧化损伤情况。结果:与对照组相比,40μmol/LCdCl_(2)处理小鼠胚胎肝细胞(BNL CL.2)12 h后,可极显著的抑制其活力(P<0.01)。显微镜下观察发现,40μmol/L CdCl_(2)处理BNL CL.2细胞12 h后,大量细胞开始出现空泡变性、核皱缩等病理改变;与对照组相比,40μmol/LCdCl_(2)处理BNL CL.2细胞6 h后,SOD活力极显著降低(P<0.01),同时染镉细胞内MDA的含量极显著升高,表明染镉处理可造成BNL CL.2细胞氧化应激损伤。结论:CdCl_(2)可诱导BNL CL.2细胞发生氧化应激损伤进而导致细胞死亡。Objective:To investigate the mechanisms of cadmium(Cd)-induced hepatotoxicity in mice.Methods:The cell viability was detected by CCK-8,then the hematoxylin-eosin staining(H&E) and Hoechst 33342 staining were used to observe the pathological changes of mice liver cells,finally the content of SOD and MDA were detected to evaluate Cd-induced oxidative damage in hepatocytes.Results:Compared with the control group,the cell viability was significantly inhibited after 12 h of 40 μmol/L CdCl_(2)exposure.After HE staining and Hoechst 33342 staining,the results showed that there was a large number of cells with vacuolar degeneration and nuclear shrinkage after 12 h of treatment with 40 μmol/L CdCl_(2).Compared with the control group,40 μmol/L CdCl_(2)after 6 h of treatment of BNL CL.2 cells,SOD activity was significantly reduced(P<0.01),and the content of MDA in cadmium-exposed cells was extremely significantly increased,indicating that cadmium exposure induces oxidative stress damage to BNL CL.2 cells.Conclusion:CdCl_(2)can induce oxidative stress damage and lead to cell death in BNL CL.2 cells.
关 键 词:镉 肝损伤 氧化应激 BNL CL.2小鼠胚胎肝细胞
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