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首页> 外文期刊>Lipids in Health Disease >Effects of 9cis,11trans and 10trans,12cis CLA on osteoclast formation and activity from human CD14+ monocytes
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Effects of 9cis,11trans and 10trans,12cis CLA on osteoclast formation and activity from human CD14+ monocytes

机译:9cis,11trans和10trans,12cis CLA对人CD14 +单核细胞破骨细胞形成和活性的影响

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Background Mixed CLA isomers variably affect bone resorption in animals and decrease osteoclast formation and activity in murine osteoclasts. These variable effects may be due to the different isomers present in commercial preparations of CLA, and the effects of the predominant individual isomers, 9cis,11trans (9,11) and 10trans,12cis (10,12) CLA are not clear. The objectives of this study were to determine the effects of the individual CLA isomers on osteoclast formation and activity from human CD14+ monocytes, and to determine whether any changes are accompanied by changes in cathepsin K, matrix metalloproteinase-9 (MMP-9), receptor activator of NF-κB (RANK) and tumour necrosis factor alpha (TNFα) gene expression. Osteoclasts were identified as TRAP+ multinucleated cells. Osteoclast activity was quantified by the amount of TRAP in the cultured media. Results At 50 μM, 9,11 CLA inhibited osteoclast formation by ~70%, and both 9,11 and 10,12 CLA decreased osteoclast activity by ~85–90%. Both isomers inhibited cathepsin K (50 μM 9,11 by ~60%; 10,12 by ~50%) and RANK (50 μM 9,11 by ~85%; 50 μM 10,12 by ~65%) expression, but had no effect on MMP-9 or TNFα expression. Conclusion 9,11 CLA inhibits osteoclast formation and activity from human cells, suggesting that this isomer may prevent bone resorption in humans. Although 10,12 CLA did not significantly reduce osteoclast formation, it reduced osteoclast activity and cathepsin K and RANK expression, suggesting that this isomer may also affect bone resorption.
机译:背景混合的CLA异构体会不同程度地影响动物的骨吸收,并降低破骨细胞的形成和鼠破骨细胞的活性。这些可变作用可能是由于CLA的商业制剂中存在不同的异构体引起的,尚不清楚主要的单个异构体CLA 9cis,11trans(9,11)和10trans,12cis(10,12)的作用。这项研究的目的是确定单个CLA异构体对破骨细胞形成和人类CD14 +单核细胞活性的影响,并确定组织蛋白酶K,基质金属蛋白酶9(MMP-9),受体是否发生变化激活NF-κB(RANK)和肿瘤坏死因子α(TNFα)基因的表达。破骨细胞被鉴定为TRAP +多核细胞。通过培养基中TRAP的量定量破骨细胞活性。结果在50μM时,9.11 CLA抑制破骨细胞形成约70%,而9,11和10,12 CLA均使破骨细胞活性降低约85-90%。两种异构体均抑制组织蛋白酶K(50μM9,11约60%; 10,12约50%)和RANK(50μM9,11约85%; 50μM10,12约65%)表达,但对MMP-9或TNFα表达无影响。结论9,11 CLA抑制破骨细胞的形成和人类细胞的活性,表明该异构体可能阻止人类的骨吸收。尽管10,12 CLA并未显着减少破骨细胞的形成,但降低了破骨细胞的活性以及组织蛋白酶K和RANK的表达,表明该异构体也可能影响骨吸收。

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