Intestinal Absorption of Luteolin from Peanut Hull Extract Is More Efficient than That from Individual Pure Luteolin

Abstract

Luteoin is one of the main flavones and the crucial effective component of peanut hull extract (PHE). The present paper aims to elucidate the absorption mechanism of luteolin and clarify whether its absorption occurs primarily at a specific site of the intestine by an in situ single-pass intestinal perfusion (SPIP) model. Moreover, the paper investigates the difference in absorption of luteolin when it is administered in PHE form and as pure luteolin by the SPIP model and in vivo pharmacokinetics studies. Results showed that the effective permeability ( P eff) and absorption rate constant ( k a) of pure luteolin(5.0 microg/mL) in duodenum and jejunum were not significantly different, but markedly higher than that in the colon and ileum. The P eff and k a of luteolin in jejunum were concentration-independent, and the ATP inhibitor (DNP) did not influence P eff and k a of pure luteolin. However, the P eff and k a of luteolin in PHE were significantly greater than that of pure luteolin. The pharmacokinetics study showed that following oral administration of a single dose of pure luteolin (14.3 mg/kg) or PHE (= 14.3 mg/kg of luteolin) in rats, the peak concentration of luteolin in plasma ( C max) and the area under the concentration curve (AUC) for pure luteolin were 1.97 +/- 0.15 microg/mL and 10.7 +/- 2.2 microg/mL.h, respectively. These parameters were significantly lower than those of the PHE group ( P < 0.05), C max = 8.34 +/- 0.98 microg/mL and AUC = 20.3 +/- 1.3 microg/mL.h, respectively. It can be concluded that luteolin is absorbed passively in the intestine of rats and that its absorption is more efficient in the jejunum and duodenum than in the colon and ileum. The bioavailability of luteolin in PHE form is significantly greater than that of pure luteolin.

Identification of the Flavonoid Luteolin as a Repressor of the Transcription Factor Hepatocyte Nuclear Factor 4α

“…In addition, there is a possibility that the plasma concentrations of luteolin cannot reach sufficient levels to affect certain gene expression. It has been reported that after administration of 14.3 mg/kg luteolin or 92.3 mg/kg peanut hull extract (equivalent to 14.3 mg/kg luteolin) by oral gavage in rats, the maximum plasma concentration of luteolin reached 1.97 g/ml (6.88 M) or 8.34 g/ml (29.1 M) (40). In the present study, we used different methods to administer luteolin to the mice.…”

Preparation and characterization of monomethoxy poly(ethylene glycol)-poly(&epsilon;-caprolactone) micelles for the solubilization and in vivo delivery of luteolin

“…6,[10][11][12][13][14][15][16][17] Moreover, Lu has cytotoxicity in cancer cells or immortalized cells, but not in normal cells, meaning that it has fewer side effects when used in treating cancer. 8,12,18 Yet Lu has some drawbacks, such as poor water solubility (,2 × 10 −2 µmol/mL), 19 low oral absorption, 20 and bioavailability (30.4% in rats), 21 which limit its clinical application. Therefore, it is of interest to promote an injectable aqueous formulation for Lu.…”

Role of Catechol-O-Methyltransferase in the Disposition of Luteolin in Rats

“…In general, the aglycone of luteolin can be directly absorbed in the intestine through passive diffusion, whereas the glycosides of luteolin will be absorbed after being hydrolyzed in the intestine by microbacteria or lactase phlorizin hydrolase (Shimoi et al, 1998;Sesink et al, 2003;Kottra and Daniel, 2007;Lu et al, 2010). It has been proved that luteolin was mainly absorbed in the jejunum passively in a single-pass perfused rat intestinal model (Zhou et al, 2008), and luteolin was relatively permeable (with a apparent permeability coefficient of 5.8 Ϯ 0.1 ϫ 10 Ϫ6 cm/s) in a Caco-2 cell model (Ng et al, 2004), which indicated moderate (20 -70%) absorption (Yee, 1997). Because of its polyphenol structure, luteolin is a good substrate of uridine diphosphate glucuronosyltransferases and sulfotransferases and mainly undergoes glucuronidation and sulfation during passage through the intestinal mucosa or the liver (Shimoi et al, 1998).…”