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亚油酸会损害鸡软骨细胞原代培养物中的胶原蛋白合成。

Linoleate impairs collagen synthesis in primary cultures of avian chondrocytes.

作者信息

Watkins B A, Xu H, Turek J J

机构信息

Department of Food Science, Lipid Chemistry, Purdue University, West Lafayette, Indiana 47907-1160, USA.

出版信息

Proc Soc Exp Biol Med. 1996 Jun;212(2):153-9. doi: 10.3181/00379727-212-44003.

DOI:10.3181/00379727-212-44003
PMID:8650253
Abstract

The effects of supplemental fatty acids, vitamin E (VIT E), and iron-induced oxidative stress on collagen synthesis, cellular injury, and lipid peroxidation were evaluated in primary cultures of avian epiphyseal chondrocytes. The treatments included oleic and linoleic acids (O or 50 microM) complexed with BSA and dl-alpha-tocopheryl acetate (VIT E at 0 or 100 microM). After 14 days of preculture, the chondrocytes were enriched with fatty acids for 8 days then cultured with VIT E for 2 days. The chondrocytes were then treated with ferrous sulfate (O or 20 microM) for 24 hr to induce oxidative stress. Collagen synthesis was the lowest and the activity of lactate dehydrogenase (LDH) was the highest in chondrocyte cultures treated with 50 microM linoleic acid and 0 VIT E. In contrast, VIT E supplemented at 100 microM partially restored collagen synthesis in the chondrocytes enriched with linoleic acid and lowered LDH activity in the media. The iron oxidative inducer significantly increased the values of thiobarbituric acid-reactive substances (TBARS) in the culture medium. The data showed that linoleic acid impaired chondrocyte cell function and caused cellular injury but that VIT E reversed these effects. Results from a previous study demonstrated that VIT E stimulated bone formation in chicks fed unsaturated fat, and the present findings in cultures of epiphyseal chondrocytes suggest that VIT E is important for chondrocyte function in the presence of polyunsaturated fatty acids. VIT E appears to be beneficial for growth cartilage biology and in optimizing bone growth.

摘要

在禽骨骺软骨细胞原代培养中,评估了补充脂肪酸、维生素E(VIT E)以及铁诱导的氧化应激对胶原蛋白合成、细胞损伤和脂质过氧化的影响。处理包括与牛血清白蛋白络合的油酸和亚油酸(O或50微摩尔)以及dl-α-生育酚乙酸酯(VIT E为0或100微摩尔)。预培养14天后,软骨细胞用脂肪酸富集8天,然后用VIT E培养2天。然后用硫酸亚铁(O或20微摩尔)处理软骨细胞24小时以诱导氧化应激。在用50微摩尔亚油酸和0 VIT E处理的软骨细胞培养物中,胶原蛋白合成最低,乳酸脱氢酶(LDH)活性最高。相比之下,补充100微摩尔的VIT E可部分恢复富含亚油酸的软骨细胞中的胶原蛋白合成,并降低培养基中的LDH活性。铁氧化诱导剂显著增加了培养基中硫代巴比妥酸反应性物质(TBARS)的值。数据表明,亚油酸损害软骨细胞功能并导致细胞损伤,但VIT E可逆转这些作用。先前一项研究的结果表明,VIT E可刺激喂食不饱和脂肪的雏鸡的骨形成,而目前在骨骺软骨细胞培养中的发现表明,在多不饱和脂肪酸存在的情况下,VIT E对软骨细胞功能很重要。VIT E似乎对生长软骨生物学和优化骨骼生长有益。

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