Recent Medline Abstracts on Herbal Medicine

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Hi All,

 

See recent Medline Abstracts on Herbal Medicine, below.

 

Phil

 

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>.

 

J Biomed Sci. 2003;10(5):518-525. Scoparone Inhibits Tissue Factor

Expression in Lipopolysaccharide-Activated Human Umbilical Vein Endothelial

Cells. Lee YM, Hsiao G, Chang JW, Sheu JR, Yen MH. Department of

Pharmacology, National Defense Medical Center, Taipei, Taiwan, ROC. Tissue

factor (TF) is an important regulator and effector molecule of coagulation in

various inflammatory states. In sepsis, expression of TF by activated

endothelial cells leads to disseminated intravascular coagulation. Scoparone is

extracted from the traditional Chinese herb ARTEMISIA SCOPARIA and is

known to have potent anti-inflammatory properties. In the current studies, we

examined the effects of scoparone on inhibiting lipopolysaccharide (LPS)-

induced TF expression in cultured human umbilical vein endothelial cells

(HUVECs). Flow-cytometric analysis revealed LPS (10 microg/ml)-activated

surface TF induction was concentration-dependently inhibited by scoparone (10-

400 microM). The concentrations of scoparone used in this study did not affect

cell viability. The elevation of the procoagulant activity of TF by LPS was

suppressed by scoparone. The LPS-induced superoxide formation was

markedly decreased by scoparone. Messenger RNA expression of TF in LPS-

activated HUVECs was also reduced by scoparone. Furthermore, scoparone

did not significantly affect the IkappaBalpha degradation. Our results

demonstrate that the inhibition of scoparone on LPS-induced TF expression in

HUVECs may mediate by the mechanisms suppressing superoxide anion

formation and TF transcription. Copyright 2003 National Science Council, ROC

and S. Karger AG, Basel PMID: 12928592 [PubMed - as supplied by publisher]

 

 

Pharmacology. 2003 Oct;69(2):79-87. Characterization of the Effect of

EPILOBIUM Extracts on Human Cell Proliferation. Vitalone A, McColl J,

Thome D, Costa LG, Tita B. Department of Pharmacology of Natural

Substances and General Physiology, University of Roma 'La Sapienza', Rome,

Italy. We have previously shown that extracts of different EPILOBIUM species,

a phytotherapeutic agent used in folk medicine as a treatment for benign

prostatic hyperplasia, inhibit proliferation of human prostate cells. The

selectivity of this effect was evaluated in four different human cell lines

(PZ-HPV-

7, normal prostate cells; LNCaP, transformed prostate cells; HMEC, mammary

cells, and 1321N1, astrocytoma cells). Different extracts of EPILOBIUM

species (E. ROSMARINIFOLIUM, E. SPICATUM, and E. TETRAGONUM) had

similar growth-inhibitory effects in all cell lines tested, indicating a lack of

specificity for prostate cells. Inhibition of DNA synthesis was mostly due to

the

nonpolar fraction of the extracts which is expected to contain flavonoids and

sterols. Polar fractions were devoid of activity with the exception of that from

E.

ROSMARINIFOLIUM. This species is the most potent in the antiproliferative

effect and contains the highest concentration of oenothein B, a hydrolyzable

ellagitannin. Oenothein B inhibited DNA synthesis in all four cell lines tested.

Extracts of E. ANGUSTIFOLIUM (the Linne denomination of E. SPICATUM)

and of E. SPICATUM from different sources were compared for their ability to

inhibit DNA synthesis and for their oenothein B content. The E.

ANGUSTIFOLIUM extract contained an amount of oenothein B 40-fold higher

than the other extract of the same species and was ten times more potent in

inhibiting DNA synthesis in a human prostate cell line. These results indicate

that EPILOBIUM extracts inhibit proliferation of prostate cells in a nonspecific

manner. Oenothein B may play a role in this effect, but other active compounds

are also present. The difference observed between extracts from the same

species underscores the importance of determination and standardization of

active ingredients in phytotherapeutic agents. Copyright 2003 S. Karger AG,

Basel PMID: 12928581 [PubMed - in process]

 

Bioorg Med Chem. 2003 Sep 1;11(18):4069-81. Synthesis of daidzin analogues

as potential agents for alcohol abuse. Gao GY, Li DJ, Keung WM. Center for

Biochemical and Biophysical Science and Medicine and Department of

Psychiatry at Massachusetts Mental Health Center, Harvard Medical School,

MA 02115, Boston, USA Daidzin, the active principle of in Gegen - Radix

puerariae and an herbal remedy for 'alcohol addiction', has been shown to

reduce alcohol consumption in all laboratory animals tested to date. Correlation

studies using structural analogues of daidzin suggests that it acts by raising

the monoamine oxidase (MAO)/mitochondrial aldehyde dehydrogenase (ALDH-

2) activity ratio (J. Med. Chem. 2000, 43, 4169). Structure-activity

relationship

(SAR) studies on the 7-O-substituted analogues of daidzin have revealed

structural features important for ALDH-2 and MAO inhibition (J. Med. Chem.

2001, 44, 3320). We here evaluated effects of substitutions at 2, 5, 6, 8, 3'

and

4' positions of daidzin on its potencies for ALDH-2 and MAO inhibition. Results

show that analogues with 4'-substituents that are small, polar and with

hydrogen bonding capacities are most potent ALDH-2 inhibitors, whereas those

that are non-polar and with electron withdrawing capacities are potent MAO

inhibitors. Analogues with a 5-OH group are less potent ALDH-2 inhibitors but

are more potent MAO inhibitors. All the 2-, 6-, 8- and 3'-substituted analogues

tested so far do not inhibit ALDH-2 and/or have decreased potencies for MAO

inhibition. This, together with the results obtained from previous studies,

suggests that a potent antidipsotropic analogue would be a 4',7-disubstituted

isoflavone. The 4'-substituent should be small, polar, and with hydrogen bonding

capacities such as, -OH and -NH(2); whereas the 7-substituent should be a

straight-chain alkyl with a terminal polar function such as -(CH(2))(n)-OH with

2</=n </=6, -(CH(2))(n)-COOH with 5</=n </=10, or -(CH(2))(n)-NH(2) with n

>/=4. PMID: 12927869 [PubMed - in process]

 

Shock. 2003 Sep;20(3):264-8. Magnolol alters cytokine response after

hemorrhagic shock and increases survival in subsequent intraabdominal sepsis

in rats. Shih HC, Wei YH, Lee CH. *Institute of Clinical Medicine, National

Yang-Ming University, Taipei, Taiwan; and dagger Department of Emergency,

Veterans General Hospital-Taipei, Taipei, Taiwan. Magnolol [from Houpo - Cx

Magnoliae officinalis] is a Chinese herbal ingredient with potent antioxidant

effects. This study evaluated the effect of magnolol in the treatment of severe

injury using a two-hit model in Sprague-Dawley rats. Hemorrhagic shock

followed by resuscitation was performed. Intra-abdominal sepsis was induced

by cecal ligation puncture. The rats were randomly segregated into the following

three groups: group 1 (sham group) rats were sham-operated; group 2

(untreated group) rats received hemorrhagic shock and resuscitation and cecal

ligation puncture 24 h later; and group 3 (treated group) rats were treated with

magnolol and subjected to the same procedures as group 2. Plasma cytokine

levels and tissue cytokine contents of lung, including tumor necrosis factor

alpha (TNFalpha) and interleukin (IL)-10 were assayed after hemorrhagic shock

and sepsis. Pulmonary injury study was performed using Evans blue dye and

survival analysis was performed after development of sepsis. Plasma and tissue

TNFalpha levels increased after hemorrhagic shock. Magnolol treatment blunted

the TNFalpha levels in plasma and tissue. The plasma IL-10 level increased

after hemorrhagic shock, whereas the tissue level of IL-10 did not change.

Magnolol treatment did not alter the plasma level of IL-10 but did increase

tissue level. After sepsis, TNFalpha levels in both plasma and tissue of

magnolol-treated animals were significantly lower than those in untreated

animals, whereas plasma and tissue IL-10 levels were not significantly different

between treated and untreated groups. Pulmonary injury study showed that

magnolol-treated rats had decreased pulmonary permeability after the onset of

sepsis. Survival analysis showed that survival rate was significantly higher in

the treated group. In conclusion, magnolol modifies the cytokine response after

hemorrhagic shock and resuscitation; the proinflammatory cytokine response is

suppressed. The modified cytokines response induced by magnolol may result

in decreased tissue injury and increased survival in subsequent intra-abdominal

sepsis. PMID: 12923499 [PubMed - in process]

 

 

 

 

 

 

 

 

 

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