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作 者:田超 王玥 李吉平 王声远 夏冰 杨越 李昶 王琪 吴永会 Tian Chao , Wang Yue , Li Jiping, Wang Shengyuan, Xia Bing, Yang Yue , Li Chang, Wang Qi, Wu Yonghui.(School of Public Health, Harbin Medical University, Harbin 150081, Chin)
机构地区:[1]哈尔滨医科大学公共卫生学院劳动卫生与职业病学教研室,150081
出 处:《中华劳动卫生职业病杂志》2018年第3期161-164,共4页Chinese Journal of Industrial Hygiene and Occupational Diseases
基 金:国家自然科学基金(81372965);国家自然科学基金(81673138)
摘 要:目的研究抗坏血酸(Ascorbic acid,AA)对镍染毒小鼠胚胎成纤维细胞(NIH/3T3)P53、Bcl-2蛋白表达的影响。方法研究采用染毒浓度为50μg/mL镍精炼尘诱导建立损伤模型,通过测定细胞相对存活率、超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)和谷胱甘肽过氧化物酶(GsH-Px)活力、过氧化氢(H2O2)和丙二醛(MDA)含量以及p53(野生型)、Bcl-2蛋白表达情况,探讨不同剂量抗坏血酸(25、50、100mmol/L)对镍精炼尘诱导NIH/3T3细胞损伤的保护作用。结果抗坏血酸Ⅲ组可以使NIH/3T3细胞存活率显著提高;细胞凋亡率降低;SOD和GSH—Px的活力明显增加,差异有统计学意义(P〈0.05);同时可以使MDA和H202水平,以及细胞外LDH酶活力明显降低,差异有统计学意义(P〈0.05)。抗坏血酸Ⅱ、Ⅲ组Bcl-2蛋白表达水平均高于镍精炼尘组,差异有统计学意义(P〈0.05);抗坏血酸各剂量组p53蛋白表达水平均低于镍精炼尘组,差异有统计学意义(P〈0.05)。结论随着抗坏血酸浓度的增加,氧化损伤水平降低,抗氧化酶水平上升,细胞凋亡减少,p53表达降低,Bcl-2表达增加,表明抗坏血酸对镍精炼尘染毒NIH/3T3细胞损伤具有一定的保护作用。Objective To study the protective effect of Ascorbic acid (AA) on the injury of nickel- exposed mouse embryonic fibroblasts (NIH/3T3). Methods A model of damage induced by 50 μg/mL nickel refining dust was established to determine the relative survival rate of cells, superoxide dismutase (SOD), lactate dehydrogenase (LDH) and glutathione peroxidase. (GSH-Px) activity, hydrogen peroxide (H202) and malondialdehyde (MDA) content, and p53 (wild-type), Bcl-2 protein expression. To investigate the protective effect of different doses of ascorbic acid (25, 50, 100 mmol/L) on nickel-refined dust-induced NIH/3T3 cell injury. Results The study showed that ascorbic acid III group can make the NIH/3T3 cell survival rate increased significantly; Apoptosis rate was reduced; The vitality of SOD and GSH-Px increased significantly, and the difference was statistically significant (P〈0.05). At the same time, the level of MDA and H202 and the activity of extracellular LDH enzyme were significantly reduced, and the difference was statistically significant (P〈0.05). The results showed that nickel refining dust induced cell damage through up-regulation of p53 protein and down-regulation of Bcl-2 protein expression ; ascorbic acid interventions, the expression level of Bcl-2 protein in ascorbic acid II and III groups was higher than that of nickel refining dust group, and the difference was statistically significant (P〈0.05) ; The expression level of p53 protein in each dose group of ascorbic acid was lower than that of nickel refined dust group, and the difference was statistically significant (P〈0.05). Conclusion With the increase of concentration of aseorbic acid, oxidative damage levels, antioxidant enzyme levels, reduce cell apoptosis, reduce expression of p53, increased expression of Bcl-2. It showed that aseorbie acid had protective effect on NIH/3T3 cell injury induced by nickel refining dust.
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