| 石浩，丁仁惠，黄谦，等.富硒油茶籽油对H2O2诱导HaCaT细胞氧化损伤的保护作用研究[J].中国油脂,2019,44(1):.[SHI Hao, DING Renhui, HUANG Qian，etc.Protective effect of selenium rich oil-tea camellia seed oil on HaCaT cell injuried by hydrogen peroxide[J].China Oils and Fats,2019,44(1):.] |
| 富硒油茶籽油对H2O2诱导HaCaT细胞氧化损伤的保护作用研究 |
| Protective effect of selenium rich oil-tea camellia seed oil on HaCaT cell injuried by hydrogen peroxide |
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| DOI： |
| 中文关键词: 油茶籽油 H2O2诱导 HaCaT细胞损伤 保护作用 |
| 英文关键词:oil-tea camellia seed oil H2O2 induction HaCaT cell injury protective effect |
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| 中文摘要: |
| 探究油茶籽油对过氧化氢诱导人永生化表皮细胞(HaCaT)氧化损伤的保护作用。以油茶果经物理压榨所得油茶籽油为材料，以体外培养的HaCaT细胞为试验对象，试验分为空白对照组、过氧化氢（H2O2）模型损伤组、阳性对照组（VC）、处理组（油茶籽油5~500 μg/mL预处理），以细胞内细胞存活率（凋亡率）、SOD、GSH-PX、ROS及其Nrf2基因表达水平为综合评价指标，评价油茶籽油的抗氧化性。结果表明：当加入油茶籽油对细胞进行预保护后，质量浓度50~200 μg/mL的油茶籽油对损伤细胞的存活率在70%~82%之间，较H2O2模型损伤组的高。50 μg/mL油茶籽油处理组细胞凋亡率为4.49%，较H2O2模型损伤组降低了44.77%；细胞内SOD水平（22.09 U/mg）、GSH-PX水平（64.50 U/mg）较H2O2模型损伤组升高了46.68%、63.66%，且存在明显差异(P＜0.05)；而ROS水平显著下降，与H2O2模型损伤组（88.27）相比细胞内平均荧光强度下降了3766%；此时Nrf2基因相对表达量为1.13，较模型组提高了101.78%；各指标均较优于阳性对照50 μg/mL VC处理组的效果。说明油茶籽油对H2O2造成的氧化损伤具有一定的预保护作用，且好于相同质量浓度的VC处理效果，可进一步将其开发成相应的天然有效抗氧化剂产品。 |
| 英文摘要: |
| The protective effect of oil-tea camellia seed oil on the human immortalized epidermal cells (HaCaT) injuried by hydrogen peroxide was studied. The oil-tea camellia seed oil from Camellia oleifera obtained by physical pressing was used as material. HaCaT cells cultured in vitro were used as the experimental objects. The experiment was divided into control group, H2O2 model damage group, positive control group (VC), and treatment group (oil-tea camellia seed oil, 5-500 μg/mL), using cell survival rate（apoptosis rate） in cell, SOD level, GSH-PX level, ROS level and Nrf2 gene expression as evaluation indexes to evaluate the antioxidant activity. The results showed that when oil-tea camellia seed oil was added to pre-protect the cells, the survival rate of damaged cells was 70%-82% for 50-200 μg/mL of oil-tea camellia seed oil, higher than H2O2 model group. The apoptosis rate of 50 μg/mL oil-tea camellia seed oil treatment group was 4.49%, reducing by 4477% compared with H2O2 model damage group. Compared with H2O2 model damage group, the levels of intracellular SOD (22.09 U/mg) and GSH-PX (64.50 U/mg) increased by 46.68% and 6366% respectively, with significant differences (P<005). While the level of ROS decreased significantly, the mean fluorescence intensity in cells decreased by 37.66% compared with H2O2 model damage group (88.27). At the same time, the relative expression of Nrf2 gene was 1.13, increasing by 10178% compared with H2O2 model damage group. All indexes were better than those of positive control 50 μg/mL VC treatment group. It indicated that oil-tea camellia seed oil had a certain pre-protective effect on oxidative damage caused by H2O2, better than the same mass concentration of VC. It could be further developed into a natural and effective antioxidant product. |
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