文章摘要
张佳婵;王昌涛;易思雨;王蕴涵;赵 丹;孙宝国.沙棘粕提取物对H2O2诱导的B16F10细胞氧化损伤的保护及修复[J].中国食品学报,2019,19(8):13-21
沙棘粕提取物对H2O2诱导的B16F10细胞氧化损伤的保护及修复
  
DOI:
中文关键词: 沙棘粕提取物  H2O2  氧化损伤模型  保护  修复
英文关键词: sea buckthorn seed residues  H2O2  oxidative damage model  protection  prothetic capability
基金项目:国家自然科学基金面上项目(31571801)
作者单位
张佳婵;王昌涛;易思雨;王蕴涵;赵 丹;孙宝国 北京食品营养与人类健康高精尖创新中心北京工商大学北京100048北京工商大学理学院植物资源研究开发北京市重点实验室北京100048北京工商大学食品学院食品添加剂与配料北京高校工程研究中心北京100048 
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中文摘要:
      研究了沙棘粕提取物(SBSE)对B16F10细胞氧化应激损伤的保护及修复作用。首先建立了过氧化氢(H2O2)诱导的B16F10细胞氧化损伤模型,完成了流式细胞术对损伤模型的评价;其次,研究了SBSE预处理对细胞防御H2O2诱导的氧化损伤细胞活力的影响,以及对损伤模型的修复作用;再次,比较了各SBSE处理组与模型组细胞谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性以及丙二醛(MDA)水平。结果:H2O2的诱导条件为300 μg/mL处理4 h,流式细胞术检测发现,H2O2处理4 h后活细胞百分比由(91.61 ± 1.14)%降至(49.77 ± 2.74)%(P<0.01),早期凋亡细胞由(1.97 ± 0.34)%升至(17.91 ± 3.55)%(P<0.01),晚期凋亡率升至(21.24 ± 2.61)%,并且H2O2处理6 h的晚期凋亡细胞显著上升,晚期凋亡率在60%以上。利用H2O2刺激SBSE预处理后的B16F10细胞,结果发现0.10 mg/mL SBSE处理后的细胞活力显著高于模型组(P<0.05),抗氧化酶活力显著提升,细胞内MDA的积累显著降低;不同浓度SBSE处理损伤模型,0.10 mg/mL SBSE具有一定的修复作用(P<0.05),其GSH-Px、CAT和SOD活力显著高于模型组(P<0.05,P<0.01,P<0.01),MDA水平显著降低(P<0.05)。由此可见,SBSE通过提高细胞GSH-Px、CAT 和SOD的活性,降低过氧化产物MDA的含量来保护和修复H2O2诱导的B16F10细胞氧化损伤。
英文摘要:
      The protective and prothetic effect of sea buckthorn seed extracts (SBSE) on oxidative damage in B16F10 was studied. Firstly, the oxidative damage model was established by treatment with H2O2. The evaluation of the damage model was done by the flow cytometry. Secondly, cells were treated by SBSE before or after the establishment of the damage model. The cell viability was measured to discuss the protective and prothetic effects of SBSE. Thirdly, the contents of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) were studied. The results showed that the oxidative damage model was established by the treatment with H2O2(300 μg/mL) for 4 h. The flow cytometry showed that the percentage of living cells decreased from (91.61 ± 1.14)% to (49.77 ± 2.74)% (P<0.01), the percentage of early apoptotic cells rose from (1.97 ± 0.34)% to (17.91 ± 3.55)%, and the late apoptosis rate increased to (21.24 ± 2.61)%. Besides, the late apoptosis rate reached more than 60% after 6 hours’ treatment, dramatically. Cells firstly treated by SBSE and then H2O2 were used to examine the cell viability and cellular antioxidant enzymes. After the pretreatment of 0.10 mg/mL SBSE, the cell viability was increased significantly, and the levels of cellular antioxidant enzymes were also increased (P<0.05). Besides, the pretreatment of SBSE could decrease the release of MDA(P<0.05). The prothetic effect of SBSE was detected when the damage model cells treated by SBSE of 0.10 mg/mL(P<0.05). The treatment of SBSE on the model could increase the activities of GSH-Px, CAT and SOD (P<0.05, P<0.01, P<0.01), and decrease the level of MDA(P<0.05), significantly. In conclusion, SBSE showed protective and prothetic effects against H2O2 induced oxidative damage in B16F10 through increasing the activities of GSH-Px, CAT and SOD, and inhibiting MDA contents.
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