CAJ | 학술논문

目的探讨乙苯对大鼠肾小管上皮细胞NRK-52e的氧化损伤及凋亡的影响.方法体外培养的NRK-52e细胞暴露于30、60、90、120μmol/L的乙苯24 h后,观察NRK-52e细胞形态和存活情况,用MTT法测定NRK-52e细胞的存活率,检测NRK-52e细胞内丙二醛(MDA)、谷胱甘肽(GSH)的含量及谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的酶活力变化,并应用PI荧光活性染色检测乙苯致NRK-52e细胞的凋亡率.结果 30 μmol/L染毒剂量组与对照组相比,其形态学改变无明显差异,60 μmol/L及90 μmol/L染毒剂量组细胞轮廓逐渐清晰,细胞折光度增强,细胞逐渐变小变圆,皱缩成球形,部分细胞破裂；120μmol/L染毒剂量组细胞大量死亡,悬浮细胞明显增多.与对照组相比,60μmol/L、90 μmol/L及120μmol/L剂量组细胞存活率及SOD活力、GSH含量、CAT活力均显著低于对照组,差异有统计学意义(P＜0.05)；90 μmol/L及120 μmol/L剂量组细胞内MDA含量及GSH-Px活力均显著低于对照组,差异有统计学意义(P＜0.05).结论乙苯可能通过降低NRK-52e细胞内CAT、GSH-Px和SOD的酶活力及GSH含量引起细胞的氧化损伤.
목적 탐토을분대대서신소관상피세포NRK-52e적양화손상급조망적영향.방법 체외배양적NRK-52e세포폭로우30、60、90、120μmol/L적을분24 h후,관찰NRK-52e세포형태화존활정황,용MTT법측정NRK-52e세포적존활솔,검측NRK-52e세포내병이철(MDA)、곡광감태(GSH)적함량급곡광감태과양화물매(GSH-Px)、초양화물기화매(SOD)、과양화경매(CAT)적매활력변화,병응용PI형광활성염색검측을분치NRK-52e세포적조망솔.결과 30 μmol/L염독제량조여대조조상비,기형태학개변무명현차이,60 μmol/L급90 μmol/L염독제량조세포륜곽축점청석,세포절광도증강,세포축점변소변원,추축성구형,부분세포파렬；120μmol/L염독제량조세포대량사망,현부세포명현증다.여대조조상비,60μmol/L、90 μmol/L급120μmol/L제량조세포존활솔급SOD활력、GSH함량、CAT활력균현저저우대조조,차이유통계학의의(P＜0.05)；90 μmol/L급120 μmol/L제량조세포내MDA함량급GSH-Px활력균현저저우대조조,차이유통계학의의(P＜0.05).결론 을분가능통과강저NRK-52e세포내CAT、GSH-Px화SOD적매활력급GSH함량인기세포적양화손상.
Objective To study the oxidative damage and apoptosis of re-nal tubular epithelial cells (NRK-52e cell line) induced by ethylbenzene.Methods NRK-52e cells were exposed to 30,60,90,120 μ mol/L ethylbenzene for 24 hours.Cell viability were measured using MTT,the activities of superoxide dismutase (SOD),glutathione peroxidase (GSH-Px) and catalase (CAT),the contents of malondialdehyde (MDA)and glutathione (GSH) were detected respectively.PI fluorescent staining assay was applied to detect percentage of apoptosis in ethylbenzene-treated groups.Results Compared with control group,cell outline became clcar,cell diopter increased,cell became smaller and shrinkage,some cells broke in 60 μmol/L ethylbenzenetreated group.Plenty of cells died,suspension cells increased significantly in 90 μmol/L ethylbenzene-treated group.Compared with control group,cell viabilitythe activities of SOD and CAT and the contentof GSH were significautly decreased in 60 and 90 μmol/L ethylbenzene-treated groups (P＜0.05).The MDA content were remarkably elevated in 90 μmol/L ethylbenzene-treated groups (P＜0.05).Conclusion ethylbenzene can induce oxidative stress and apoptosis in NRK-52e cells.