Genistein upregulates placental corticotropin-releasing hormone expression in lipopolysaccharide-sensitized mice.

Genistein is a phytoestrogen isolated from soya beans. Although soy products are staple food of Asian, the potential effect of genistein on reproduction has not been fully addressed. Lipopolysaccharide (LPS) is an endotoxin found in the cell membrane of gram-negative bacteria. It may cause inflammation and other immune responses. Previous study has shown that LPS may induce pre-mature birth in rodents. In the present study, effect of genistein on LPS-induced preterm birth was investigated. Pregnant ICR mice were gavaged with genistein at 40, 200 and 400 mg/kg body weight/day during E13 to E16. LPS was injected i.p. on E16.5 and the animals were sacrificed at E17. Compared to the control group, an increased incidence of early delivery was observed in the pooled mice under LPS treatment. A rising trend of incidence was also demonstrated dose-dependently with genistein co-treatment. Real-time RT-PCR indicated that the placental crh expression was highly induced by the co-administration of 400 mg/kg genistein and LPS. By contrast, neither genistein nor LPS alone could alter the expression. Increased plasma CRH concentration was also seen in the co-treatment groups. In addition, the mRNA expression of placental CRH-binding protein and plasma progesterone concentration were reduced in these groups. These results indicated that genistein might exacerbate the undesirable effect of LPS on pregnant mice by altering hormonal regulations.

Theaflavins in black tea and catechins in green tea are equally effective antioxidants.

Green tea catechins, including (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin gallate (EGCG), are oxidized and dimerized during the manufacture of black tea and oolong tea to form orange-red pigments, theaflavins (TF), a mixture of theaflavin (TF1), theaflavin-3-gallate (TF2A), theaflavin-3'-gallate (TF2B) and theaflavin-3,3'-digallate (TF3). The present study was designed to compare the antioxidant activities of individual TF with that of each catechin using human LDL oxidation as a model. All catechins and TF tested inhibited Cu(+2)-mediated LDL oxidation. Analysis of the thiobarbituric acid-reactive substances (TBARS) and conjugated dienes produced during LDL oxidation revealed that the antioxidant activity was in the order: TF3 > ECG > EGCG > or = TF2B > or = TF2A > TF1 > or = EC > EGC. Four TF derivatives also demonstrated a dose-dependent antioxidant activity in Cu(+2)-mediated LDL oxidation at concentrations of 5-40 micromol/L. These results demonstrate that the TF present in black tea possess at least the same antioxidant potency as catechins present in green tea, and that the conversion of catechins to TF during fermentation in making black tea does not alter significantly their free radical-scavenging activity.

Stimulation of histamine H2 receptor in rat hypothalamus releases endogenous norepinephrine.

The effect of histamine (HA) on the release of endogenous norepinephrine (NE) from superfused rat hypothalamic and striatal slices was assessed. Measurements were made by high-performance liquid chromatography with electrochemical detection. Superfusion with HA (0.1-80 microM) resulted in a concentration-dependent increase (10-220%) of NE release from hypothalamus but was ineffective in the striatum. The process was Ca++-dependent and was unaffected by blockade of monoamine oxidase. The H2 agonists, dimaprit (50 microM) and impromidine (10 microM), increased NE release from hypothalamic slices 3-fold and 2-fold, respectively. Tiotidine (10 microM), an H2 antagonist, did not alter the spontaneous release of NE but completely abolished the effect of dimaprit. To increase the ability of the tissue to sustain NE release on repeated stimulation, tyrosine was added to the perfusion medium. Under these conditions 10 microM HA produced, in two consecutive stimuli, a 1.9-fold increase. Two consecutive stimuli by 80 microM HA elicited a 3.2- and a 2.9-fold increase. Under the same conditions, 50 microM ranitidine, another H2 antagonist, but not pyrilamine, an H1 antagonist, completely blocked the effect of 10 microM HA. Although NE release was increased in the presence of tyrosine, tyrosine did not increase the tissue levels of NE. These experiments imply that H2 receptor activation increases release of NE from the rat hypothalamus. Since in the hypothalamic slice, noradrenergic nerve endings are cut from their cell bodies, the modulatory event must have occurred at the nerve terminals.