decanoylcarnitine and decanoic-acid

decanoylcarnitine has been researched along with decanoic-acid* in 3 studies

Reviews

1 review(s) available for decanoylcarnitine and decanoic-acid

ArticleYear
Mechanistic analysis for drug permeation through intestinal membrane.
    Drug metabolism and pharmacokinetics, 2007, Volume: 22, Issue:2

    For drug absorption, intestinal drug permeability's through both the paracellular and transcellular routes were analyzed. Absorption enhancers, such as sodium caprate (C10), decanoylcarnitine (DC) and tartaric acid (TA), increased the paracellular permeability of water-soluble, low lipophilic and poorly absorbable drugs by enlargement of tight junction (TJ) adhering to the intercellular portion; that is, expansion of the paracellular routes. C10 increased the intracellular calcium level to induce contraction of calmodulin-dependent actin filaments. Although DC also increased the intracellular calcium level, the action was independent of calmodulin, and thus the action mechanism of DC was considered to differ from that of C10. DC and TA decreased the intracellular ATP level and the intracellular pH, suggesting that intracellular acidosis increases the calcium level through decrease in ATP level followed by opening TJ. TA had no effect on Western blot analysis, but TA significantly inhibited excretion of rhodamine 123, one of the P-glycoprotein (P-gp) substrates, from the serosal to mucosal side, suggesting that TA increases the intestinal absorption of P-gp substrates, possibly by inhibiting the P-gp function without changing the expression of P-gp. During ischemia/reperfusion (I/R) injury during small intestine grafting, TJ opening and decrease in P-gp function simultaneously occurred. The in vitro model of I/R showed that lipid peroxidation is a trigger of the injury, and superoxide and iron ion participate in TJ opening and decrease in P-gp function. Colonic epithelial cells have the specific transcellular transport systems for lipopolysaccharide (LPS), one of which shows substrate specificity in the interaction with CD14 and/or that of TLR4. In the infective disease induced by LPS, the mucosal LPS sensitive transport capability was decreased and in the secretory direction, the receptor-mediated uptake mechanism disappeared. LPS taken up into the cells can be excreted by P-gp or mrp. The expression levels and function of the secretory transporters were considered to be increased in the infective condition. In conclusion, changes in TJ as the membrane structure and P-gp as the membrane function are important factors controlling intestinal membrane transport.

    Topics: Animals; ATP Binding Cassette Transporter, Subfamily B, Member 1; Bacterial Infections; Caco-2 Cells; Carnitine; Cell Membrane Permeability; Decanoic Acids; Drug Evaluation, Preclinical; Humans; Inflammatory Bowel Diseases; Intestinal Absorption; Intestinal Diseases; Intestinal Mucosa; Intestines; Lipid Peroxidation; Lipopolysaccharides; Pharmaceutical Preparations; Reperfusion Injury; Tartrates; Tight Junctions

2007

Other Studies

2 other study(ies) available for decanoylcarnitine and decanoic-acid

ArticleYear
Absorption-enhancing mechanism of EDTA, caprate, and decanoylcarnitine in Caco-2 cells.
    Journal of pharmaceutical sciences, 1996, Volume: 85, Issue:6

    The mechanism of paracellular expansion by absorption enhancers, e.g., EDTA, sodium caprate (C10), and decanoylcarnitine (DC), was studied, the focus being on the process of actin microfilament contraction in the tight junction. The effects of various inhibitors such as KN-62 (a specific inhibitor of Ca2+/calmodulin dependent protein kinase), H7 (a protein kinase C (PKC) inhibitor), and W7 (a calmodulin antagonist) were examined on the paracellular expansion by the enhancers in Caco-2 cells. From the experimental results, the following mechanisms were suggested. EDTA activates PKC by depletion of extracellular calcium via chelation resulting in expansion of the paracellular route. C10 increases the intracellular calcium level by an interaction with the cell membrane independent of cell polarity resulting in contraction with actin microfilament. DC interacts specifically with the apical membrane to increase the intracellular calcium level, but the mechanistic details subsequent to the increase of calcium are not clear.

    Topics: Caco-2 Cells; Calcium; Carnitine; Cell Membrane Permeability; Decanoic Acids; Dextrans; Egtazic Acid; Electric Impedance; Epithelium; Fluorescein-5-isothiocyanate; Humans; Intestinal Absorption; Intestinal Mucosa; Intracellular Fluid

1996
Absorption-enhancing mechanism of sodium caprate and decanoylcarnitine in Caco-2 cells.
    The Journal of pharmacology and experimental therapeutics, 1995, Volume: 272, Issue:2

    The mechanism of action of the absorption enhancers such as sodium caprate (C10) and decanoylcarnitine (DC) was examined. Both C10 and DC increased the epithelial permeability of fluorescein isothiocyanate dextran 4000 and decreased the transepithelial electrical resistance in Caco-2 cell monolayer. Irrespective of the presence or absence of mucosal calcium, C10 rapidly increased intracellular calcium levels dose-dependently. Compound 48/80, a phospholipase C inhibitor, prevented the increases of the intracellular calcium level and permeability of fluorescein isothiocyanate dextran 4000 by C10. Furthermore, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride, a strong calmodulin inhibitor, also significantly decreased the enhancing effect of C10. These results suggest that C10 releases calcium from intracellular stores via activation of phospholipase C in plasma membrane. The increase of the calcium levels was considered to induce the contraction of calmodulin-dependent actin microfilament, followed by dilatation of the paracellular route. Although DC also increased intracellular calcium levels, neither compound 48/80 nor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride decreased the enhancing effect of DC. The enhancing mechanisms were different for C10 and DC.

    Topics: Calcium; Carnitine; Decanoic Acids; Humans; Intestinal Absorption; Myosin-Light-Chain Kinase; p-Methoxy-N-methylphenethylamine; Permeability; Tumor Cells, Cultured; Type C Phospholipases

1995