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共轭亚油酸可降低佛波酯诱导的牛子宫内膜细胞中前列腺素F2α的产生。

Conjugated linoleic acid reduces phorbol ester-induced prostaglandin F2alpha production by bovine endometrial cells.

作者信息

Rodriguez-Sallaberry C, Caldari-Torres C, Greene E S, Badinga L

机构信息

Department of Animal Sciences University of Florida, Gainesville, Florida 32611, USA.

出版信息

J Dairy Sci. 2006 Oct;89(10):3826-32. doi: 10.3168/jds.S0022-0302(06)72424-9.

Abstract

Recent interest in conjugated linoleic acid (CLA) research stems from the well-documented anticarcinogenic, antiatherogenic, antidiabetic, and antiobesity properties of CLA in animal models. The objective of this study was to examine the effects of 2 CLA isomers (cis-9,trans-11 and trans-10,cis-12) on phorbol 12,13-dibutyrate (PDBu)-induced PGF2alpha production in cultured bovine endometrial (BEND) cells. Confluent BEND cells were incubated in the absence (control) or presence of 100 microM each of linoleic acid, cis-9,trans-11 CLA, or trans-10,cis-12 CLA for 24 h. After incubation, cells were rinsed and then stimulated with PDBu (100 ng/mL) for 6 h. Compared with untreated cells, PDBu stimulated PGF2alpha secretion (+25-fold) within 6 h. The increases in PGF(2alpha) secretion were paralleled by signifi-cant induction of prostaglandin endoperoxide synthase-2 (PGHS-2) mRNA (+63-fold) and protein (+1.6-fold) expression. In spite of stimulatory effects on PGHS-2 and peroxisome proliferator-activated receptor delta (PPARdelta) mRNA responses, CLA greatly decreased PGF2alpha production by PDBu-stimulated BEND cells. There was no evidence for PDBu or CLA modulation of PPARdelta protein synthesis in cultured BEND cells. Results indicated that CLA modulation of PGF2alpha production by BEND cells was not mediated through PGHS-2 or PPARdelta gene repression.

摘要

近期对共轭亚油酸(CLA)研究的兴趣源于其在动物模型中已被充分证明的抗癌、抗动脉粥样硬化、抗糖尿病和抗肥胖特性。本研究的目的是检测两种CLA异构体(顺式-9,反式-11和反式-10,顺式-12)对佛波醇12,13-二丁酸酯(PDBu)诱导的培养牛子宫内膜(BEND)细胞中前列腺素F2α(PGF2α)产生的影响。将汇合的BEND细胞在不存在(对照)或存在100μM亚油酸、顺式-9,反式-11 CLA或反式-10,顺式-12 CLA的情况下孵育24小时。孵育后,冲洗细胞,然后用PDBu(100 ng/mL)刺激6小时。与未处理的细胞相比,PDBu在6小时内刺激了PGF2α的分泌(增加25倍)。PGF2α分泌的增加与前列腺素内过氧化物合酶-2(PGHS-2)mRNA(增加63倍)和蛋白质(增加1.6倍)表达的显著诱导平行。尽管CLA对PGHS-2和过氧化物酶体增殖物激活受体δ(PPARδ)mRNA反应有刺激作用,但CLA大大降低了PDBu刺激的BEND细胞中PGF2α的产生。在培养的BEND细胞中没有证据表明PDBu或CLA对PPARδ蛋白合成有调节作用。结果表明,CLA对BEND细胞中PGF2α产生的调节不是通过PGHS-2或PPARδ基因抑制介导的。

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