Ki-Nam Lee

Acanthopanax senticosus root inhibits mast cell-dependent anaphylaxis.

BACKGROUND Mast cells synthesize and secrete chemical mediators which play a central role in anaphylaxis. METHODS The effect of Acanthopanax senticosus root (ASR) on mast cell-dependent anaphylaxis was investigated. RESULTS ASR inhibited compound 48/80-induced systemic anaphylactic shock at the dose of 1.0 g/kg by 50%. When ASR was given as pre-treatment at concentrations ranging from 0.01 to 2.0 g/l, the histamine release from rat peritoneal mast cells induced by compound 48/80 was reduced in a dose-dependent manner. ASR (2.0 g/kg) also inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl (DNP) IgE to 53.17+/-6.62%. Moreover, ASR inhibited tumor necrosis factor-alpha production in a concentration-dependent manner, and the treatment of 1 g/l blocked the production by 32.5+/-3.50% compared to saline value. CONCLUSIONS ASR may possess effective anti-anaphylactic activity.

Anti-inflammatory activity of Korean folk medicine purple bamboo salt.

Abstract Purple bamboo salt is a specially processed salt according to the traditional recipe using normal salt and bamboo. It has been used for the purpose of prevention and treatment of various diseases in Korea. We investigated the anti‐inflammatory activity of purple bamboo salt by using human mast cell line (HMC‐1). Purple bamboo salt (1 mg/mL) inhibited phorbol 12‐myristate 13‐acetate (PMA) plus calcium ionophore A23187‐stimulated tumor necrosis factor (TNF)‐α, interleukin (IL)‐1β and IL‐6 secretion, by 67.04% ± 0.08%, 68.01% ± 1.85%, and 69.48% ± 0.54%, respectively. In addition, the expression of TNF‐α mRNA in HMC‐1 cells was inhibited by purple bamboo salt under the same condition. When NaCl (1 mg/mL) was added, the secretion of TNF‐α and IL‐6 was also inhibited but the effect was markedly lower than purple bamboo salt. Our results suggest that purple bamboo salt importantly contributes to the prevention or treatment of inflammatory diseases.

Methyl gallate inhibits the production of interleukin-6 and nitric oxide via down-regulation of extracellular-signal regulated protein kinase in RAW 264.7 cells.

To determine the anti-inflammatory and analgesic activities of methyl gallate (MG) isolated from Galla Rhois, MG was studied in vivo for its analgesic activities using the writhing response in mice. Anti-inflammatory activity of MG was evaluated for NO and IL-6 production in RAW 264.7 cells. MG inhibited LPS-induced NO and IL-6 production. Consistent with these observations, the protein and mRNA expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were inhibited by MG. Moreover, MG suppressed the phosphorylation of ERK1/2 in LPS-induced RAW 264.7 cells in a dose-dependent manner. Taken together, the results of this study indicate that MG has anti-inflammatory effects.

Polymorphism of angiotensin-converting enzyme gene and BMI in obese Korean women

BACKGROUND The renin-angiotensin system (RAS) plays a role in the pathogenesis of metabolic diseases. This system was recently found to be completely expressed in human adipose tissue. Especially angiotensin II, the active component of RAS, may affect adipogenesis and adipocyte metabolism. We examined whether obese and non-obese subjects differ from angiotensin-converting enzyme (ACE) genotype distribution, and whether the ACE genotypes affect the anthropometric parameters or the degrees of body mass index (BMI). METHODS The study included 155 obese healthy women (BMI > or = 25 kg/m(2), range 25-54.7, age range 15-40 years), 82 non-obese women (BMI < 25 kg/m(2), range 15-40 years), and 613 random controls. Total fat mass and percent body fat (PBF) were determined by dual-energy X-ray absorptiometry (DEXA). Genomic DNA was extracted and used for polymerase chain reaction (PCR)-based genotyping of ACE. RESULTS Age, percent body fat, waist-to-hip ratio (WHR), body mass index, and cholesterol concentrations did not differ from ACE genotype. No differences were observed for allelic and genotype frequencies between obese women (BMI > or = 25) and 82 non-obese women or 613 random controls. In addition, no association of ACE polymorphism was observed with BMI for genotype in obese women. CONCLUSIONS ACE polymorphism is not a significant factor for BMI and does not contribute to the odds of obesity in obese healthy women from Korea.

Interpretation of scanning probe microscope image of the structure of atomic vacancy on graphite: ab initio periodic Hartree–Fock calculations ☆

Abstract By using the CRYSTAL 95 program, ab initio periodic Hartree–Fock (PHF) calculations with the full potential and 6-21G∗ basis set are applied to the interpretation of scanning tunneling microscope (STM) and atomic force microscopy (AFM) image of the structure of atomic vacancy in graphite. Our results show that change in the total electron density when compared with the ideal structure is considerable at the missing atom site, but it is not considerable beyond a distance upon the missing atom site. However, the partial charge density, which originates from the states near the Fermi energy is enhanced at the atoms surrounding the vacancy. These results are in a good agreement with those of Hahn et al. (Phys. Rev. B 53 (1996) R1725), who take that vacancies are transparent in AFM but imaged as surface protrusions in STM. In conclusion, our results should clarify the reason why vacant sites of graphite are visible shown in STM, while they are not easy to detect in AFM.

Tetrahydroabietic acid, a reduced abietic acid, inhibits the production of inflammatory mediators in RAW264.7 macrophages activated with lipopolysaccharide.

Abietic acid (AA), the main component of the rosin fraction of oleoresin synthesized by conifer species, has been reported to have anti-inflammatory effects. AA is a weak contact allergen; however, compounds resulting from its oxidation by air elicit stronger allergic response. Hydrogenation of the conjugated double bonds of AA, as in tetrahydroabietic acid (THAA), decreases its susceptibility to air oxidation and would thus reduce the allergenicity of AA. The aim of this study was to investigate whether THAA could exert anti-inflammatory effects to the same extent as AA in RAW264.7 macrophages activated with the endotoxin lipopolysaccharide (LPS). THAA and AA inhibited the production of nitric oxide (NO) and prostaglandin E2 by suppressing the expression of inducible NO synthase and cyclooxygenase-2, respectively, in LPS-activated RAW264.7 macrophages. They also inhibited the LPS-induced production of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. Both THAA and AA prevented the LPS-induced nuclear translocation of the nuclear factor-κB/p65 subunit, suggesting that THAA may inhibit the production of pro-inflammatory mediators through the same mechanism as AA. In comparison, the anti-inflammatory effects of THAA and AA were almost identical, indicating that THAA retains the anti-inflammatory activity of AA at least in LPS-activated RAW264.7 macrophages.

Enhancement of pentobarbital-induced sleep by apigenin through chloride ion channel activation

This experiment was performed to investigate whether apigenin has hypnotic effects and/or enhances pentobarbital-induced sleep behaviors through the GABAergic systems. Apigenin prolonged sleep time induced by pentobarbital similar to muscimol, a GABAA receptors agonist. Apigenin also increased sleep rate and sleep time in the combined administration with pentobarbital at the sub-hypnotic dosage, and showed synergic effects with muscimol in potentiating sleep onset and enhancing sleep time induced by pentobarbital. In addition, both of apigeinin and pentobarbital increased chloride influx in primary cultured cerebellar granule cells. Apigenin increased glutamate decarboxylase (GAD) and had no effect on the expression of GABAA receptorα-, β-, γ-subunits in n hippocampus of mouse brain, showing different expression of subunits from pentobarbital treatment group. In conclusion, it is suggested that apigenin augments pentobarbital-induced sleep behaviors through chloride ion channel activation.

Regioisomerism of the C60X2 (X=O, CH2, SiH2, GeH2)

Abstract The structures of eight regioisomers of 6-6 bond organic derivatives of C 60 X 2 (X=O, CH 2 , SiH 2 , GeH 2 ) with intact cages have been calculated at the semiempirical PM-3 level. For the bis-adducts of O, CH 2 , and GeH 2 , cis-1 regioisomer is the most stable among the respective regioisomers. But in the case of SiH 2 , equatorial regioisomer is the most stable and all trans-1, -2, -3, and -4 regioisomers are more stable than cis-1 regioisomer.

Hypothetical Buckminsterfullerenedithio-tetrathiafulvalene

Abstract The electronic and atomic structure of three hypothetical buckminsterfullerenedithio-tetrathiafulvalenes (C 60 DT-TTFs) regioisomers have been calculated at the level of the semiempirical Hartree-Fock molecular orbital theory. The C 60 DT-TTFs are formed by the 1,2-, 1,4- , and 2,3- cycloadditions of a cyclohexatrienyl unit of C 60 . The energies of the C 60 DT-TTFs relative to that of the most stable 1,2 -C 60 DT-TTF are 0.507 eV for the 1,4 -C 60 DT-TTF and 0.681 eV for the 2,3 -C 60 DT-TTF. All these structures show a C S symmetry. The net charge of the C 60 fragment is negative and that of the DT-TTF fragment is positive. Thus, it is interesting in that the C 60 as the electron acceptor and the DT-TTF fragment as the electron donor have combined to form the C 60 DT-TTF.

PHOSPHATIDYLINOSITOL 3-KINASE REGULATES PROLIFERATION OF RAW 264.7 MACROPHAGES

Phosphatidylinositol 3-kinase (PI3-kinase) is an enzyme that acts as a direct biochemical link between a novel phosphatidylinositol pathway and a number of proteins containing intrinsic or associated kinase activities. Here we demonstrate that wortmannin, PI3-kinase inhibitor, decreases the proliferation of RAW 264.7 macrophages and that another structurally unrelated inhibitor of PI3-kinase, LY294002, also inhibits the proliferation. These results indicate a possible involvement of PI3-kinase in RAW 264.7 macrophages growth regulation. Wortmannin stimulation of RAW 264.7 macrophages is followed by sustained expression of the mRNA of c-fos and a transient expression of the mRNA of c-jun. We also show that the wortmannin and LY294002 induce a cell cycle arrest in asynchronously growing cells leading to an inhibition of cell proliferation after 12 h of treatment. In addition, wortmannin or LY294002 inhibited the phorbol 12-myristate 13-acetate-induced macrophages proliferation potently. These results suggest that PI3-kinase plays an important role in growth regulation of RAW 264.7 macrophages and that protein kinase C is a down stream effector of PI3-kinase.