ArticleLipids2008
Conjugated linoleic acids and CLA-containing phospholipids inhibit NO formation in aortic endothelial cells.
Article in Lipids, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate.Hypertension (Dallas, Tex. : 1979) · 2017Trial
- Oral phosphatidylcholine pretreatment alleviates the signs of experimental rheumatoid arthritis.Arthritis research & therapy · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study examined the effects of five CLA isomers and the non-conjugated LA on nitric oxide (NO) production, an important modulator of vasodilation, inflammation, and cytotoxicity. Bovine aortic endothelial cells (BAECs) were pretreated with pure CLAs (c9, c11-, c9, t11-, t9, t11-, t10, c12-, c11, c13-CLA) and the non-conjugated c9, c12-analog, then stimulated by the ionophore A23187 followed by fluorescence monitoring of NO production. CLAs (5 microM) decreased NO formation in the range of 20-40% relative to non-fatty acid-treated controls with the t9, t11- and t10, c12-CLAs being the most effective. The inhibitory effect of either of these CLAs was not time dependent over a 120 min time interval. Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) play crucial roles in membrane structure and cell signaling. Since CLAs are usually esterified in these phospholipids (PLs), the effects of three CLA-containing PLs and 2-linoleoyl-PC on NO production by A23187-stimulated BAECs were also examined. c9, t11-CLA-PC and 2-linoleoyl-PC dose-dependently inhibited NO production over a 60-1,000 microM concentration range whereas c9, c11-CLA-PC and c9, t11-CLA-PE were ineffective. Both c9, t11-CLA-PC and linoleoyl-PC exhibited a time-dependent decrease in NO production from 5 to 120 min. The results of the present study suggest that the influence of several C18 polyunsaturated fatty acids incorporated into cellular phospholipids on the A23187-induced formation of NO by BAECs is strongly dependent on the positional and geometric nature of the double bonds.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.