• The Korean Journal of Mycology
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• v.21 no.1
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• pp.23-27
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• 1993

Ion effects on $11{\alpha}-hydroxylation$ of progesterone and $5{\alpha}-reduction\;of\;11{\alpha}-hydroxyprogesterone$ by Rhizopus nigricans were investigated. Metal ions such as $Cu^{2+},\;Cd^{2+},\;Co^{2+},\;Mn^{2+},\;Zn^{2+},\;Fe^{2+},\;Mg^{2+},\;Fe^{3+}\;and\;Na^+$ reduced the $11{\alpha}-hydroxylation$ activity, while $K^+$ stimulated the same reaction. Enzyme activity for the $5{\alpha}-reduction$ of $11{\alpha}-hydroxyprogesterone$ was increased in the presence of $Fe^{2+},\;Mn^{2+},\;Mg^{2+},\;Co^{2+},\;Zn^{2+},\;Fe^{3+},\;K^+\;and\;Na^+$, whereas it was decreased in the presence of $Cd^{2+}\;and\;Cu^{2+}$. Potassium ion of $10^{-3}\;M\;$ of concentration was found to be effective for the promotion of $11{\alpha}-hydroxylation$. On the other hand, cadmium ion of $10^{-4}\;M$ was proved to suppress the $5{\alpha}-reduction$ reaction. Progesterone is reported to be transformed into $11{\alpha}-hydroxyprogesterone$ which, in turn, is converted further into $11{\alpha}-hydroxy-allopregnane-3$, 20-dione by R. nigricans. From this point of view, the highest yield of $11{\alpha}-hydroxyprogesterone$ could be obtained when potassium ion of $10^{-3}\;M$ was given initially followed by addition of cadmium ion of $10^{-4}\;M$ to limit conversion of 11{\alpha}-hydroxyprogesterone into $11{\alpha}-hydroxy-allopregnane-\;3$, 20-dione.

• Journal of the Korean Chemical Society
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• v.27 no.3
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• pp.194-200
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• 1983

Effect of metallic salts added to the ${\alpha}-Fe_2O_3-HCl\;or\;{\alpha}-Fe_2O_3-H_2SO_4$ reaction systems were investigated by colorimetric and gravimetric determinations. While reductive salts exhibited remarkably enhanced reaction rate, non-reductive salts showed inhibitive results. We supposed that the improvement of dissolution rate of ${\alpha}-Fe_2O_3$ by the addition of $FeCl_2$, a reductive salt, to the ${\alpha}-Fe_2O_3-HCl$ system can be attributed to the formation of chloro-bridge between $Fe^{3+}\;and\; Fe^{2+}$, and therefore some partial electronic charge transfer from $Fe^{2+}\;to\;Fe^{3+}$ on the surface of ${\alpha}-Fe_2O_3$ will be easily achieved through the bridged bond. The transferred charge to the surface will reduce the positive charge of initial $Fe^{3+}$, and also result to reduce the lattice energy of that site. Assuming tothat there is a linear relationship between the lattice energy change and the change of activation energy of the reaction system, the transferred partial electronic charge to $Fe^{3+}$ of ${\alpha}-Fe_2O_3$ surface was calculated to be ca. 0.36e.

• Journal of Veterinary Clinics
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• v.19 no.3
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• pp.342-349
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• 2002

Vitamin D is one of important factors involved in the regulation of bone metabolism. In osteoporosis, the therapeutic effect of vitamin D on the healing process has still been controversial. To conform the effect of $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ on osteoporosis, the change of serum calcium, serum phosphorus, serum alkaline phosphatase, bone mineral density and bone mineral content of osteoporotic tibia were examined comparatively in normal control group(positive control), CFA control(negative control), CFA+$1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group and CFA+$1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group after osteoporosis was induced by single injection of complete Freund's adjuvant(CFA) in rats. In change of serum calcium. the significantly increased value was shown on 2nd and 5th week(P< 0.05) after treatment in $1{\alpha}$, 25 dihydroxy-vitamin D$_3$ 0.01 ug/kg group and on 3rd week(P<0.05) after treatment in $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than CFA control. In change of serum phosphorus, the significantly increased value was shown on 2nd week(P<0.05) after treatment in $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group and on 3rd and 4th week(P<0.05) after treatment in $1{\alpha}$, ,25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than CFA control. The value of bone mineral density and bone mineral content of tibia was increased in both $1{\alpha}$,25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group and $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than CFA control, and the increase rate of that was higher in $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.1 ug/kg group than $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ 0.01 ug/kg group. Considering above findings collectively, it was considered that $1{\alpha}$, 25 dihydroxy-vitamin $D_3$ was effective in preventing the complete Freund's adjuvant-induced osteoporotic decrease of bone mass.

• Biomedical Science Letters
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• v.14 no.1
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• pp.63-68
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• 2008

The aqueous extract from the fruit body of Lentinus edodes was evaluated for inhibitory activities against $\alpha$-glucosidase isolated from Spargue-Dawley male rats. A aqueous extract of Lentinus edodes exhibited 13.8% inhibitory activity on using 2 mM p-nitrophenyl $\alpha$-D-glucopyranoside as a substrate ($IC_{50}$ 75.3 mg/ml). The aqueous extract of Lentinus edodes inhibition type on $\alpha$-glucosidase was determined to be competitive inhibition. When it was oral administered to increase of blood glucose levels after STZ-induced in a dose dependent dietary. These results suggest that aqueous extract of Lentinus edodes effect a metabolism of intestine, and thereby reducing the increase of blood glucose after STZ-induced.

• Nutrition Research and Practice
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• v.10 no.3
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• pp.282-287
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• 2016

BACKGROUND/OBJECTIVES: Jerusalem artichoke has inhibitory activity against ${\alpha}$-glucosidase and decreases fasting serum glucose levels, which may be related to its fructan content. The biological activity of fructan can be influenced by the degree of polymerization. Thus, in this study, the inhibitory effects of original and fermented purple Jerusalem artichoke (PJA) on ${\alpha}$-glucosidase were compared in vitro. Additionally, the anti-diabetes effect of Lactobacillus plantarum-fermented PJA (LJA) was studied in a non-insulin-dependent diabetes mellitus animal model (C57BIKsJ db/db). MATERIALS/METHODS: The water extract of PJA was fermented by L. plantarum, and two strains of Bacillus subtilis to compare their anti-${\alpha}$-glucosidase activities in vitro by ${\alpha}$-glucosidase assays. The anti-diabetes effect of LJA was studied in a non-insulin-dependent diabetes mellitus animal model (C57BIKsJ db/db) for seven weeks. During the experiment, food intake, body weight, and fasting blood glucose were measured every week. At the end of the treatment period, several diabetic parameters and the intestinal ${\alpha}$-glucosidase activity were measured. RESULTS: The LJA showed the highest ${\alpha}$-glucosidase inhibitory activity in vitro. In the in vivo study, it resulted in a significantly lower blood glucose concentration than the control. Serum insulin and HDL cholesterol levels were significantly higher and the concentrations of triglycerides, non-esterified fatty acids, and total cholesterol were significant lower in mice treated with LJA after seven weeks. In addition, the intestinal ${\alpha}$-glucosidase activity was partially inhibited. CONCLUSIONS: These results suggested that LJA regulates blood glucose and has potential use as a dietary supplement.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.4
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• pp.199-205
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• 2003

Osteoblasts are affected by TNF-${\alpha}$ overproduction by immune cells during inflammation. It has been suggested that functional $NF-{\kappa}B$ sites are involved in TNF-${\alpha}$-induced bone resorption. Thus, we explored the effect of pyrrolidine dithiocarbamate (PDTC), which potently blocks the activation of nuclear factor $(NF-{\kappa}B)$, on the induction of TNF-${\alpha}$-induced activation of JNK/SAPK, AP-1, cytochrome c, caspase and apoptosis in MC3T3E1 osteoblasts. Pretreatment of the cells with PDTC blocked TNF-${\alpha}$-induced $NF-{\kappa}B$ activation. TNF-${\alpha}$-induced activation of AP-1, another nuclear transcription factor, was suppressed by PDTC. The activation of c-Jun N-terminal kinase, implicated in the regulation of AP-1, was also down regulated by PDTC. TNF-${\alpha}$-induced apoptosis, release of cytochrome c and subsequent activation of caspase-3 were abolished by PDTC. TNF-${\alpha}$-induced apoptosis was partially blocked by Ac-DEVD-CHO, a caspase-3 inhibitor, suggesting that caspase-3 is involved in TNF-${\alpha}$-mediated signaling through $NF-{\kappa}B$ in MC3T3E1 osteoblasts. Thus, these results demonstrate that PDTC, has an inhibitory effect on TNF-${\alpha}$-mediated activation of JNK/SAPK, AP-1, cytochrome c release and subsequent caspase-3, leading to the inhibition of apoptosis. Our study may contribute to the treatment of TNF-${\alpha}$-associated immune and inflammatory diseases such as rheumatoid arthritis and periodontal diseases.

• Bulletin of the Korean Chemical Society
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• v.30 no.12
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• pp.3053-3056
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• 2009

The title compound, ${\alpha},{\alpha}$-dichloro-o-methylacetophenone, was prepared and its photochemical behavior was investigated. Addition of an extra chlorine at alpha position to the carbonyl showed many different features from photochemical reactivities of mono chloro analogue, 2,5-dimethylphenacyl chloride. In benzene, a rearrangement product with a formal 1,5-Cl shift and a reduction product were formed beside indanone. In methanol, solvolysis and cyclization of a common dienol intermediate occurred at comparable reaction rates.

• Environmental Analysis Health and Toxicology
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• v.9 no.1_2
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• pp.25-35
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• 1994

Many nephrotoxic agents exert their effect primarily on the cells of the proximal tubules. We used the LLC-$PK_1$, kidney epithelial cell line as a model system for studies on nephrotoxicity and investigated whether the uptake of $\alpha$-methylglucose($\alpha$-MG) could serve as a parameter to assess effects of nephrotoxicants on the functional integrity of the cells at an early time of toxicity. The enzyme leakage test which has been used to be as a conventional cytotoxic parameter in vitro, was conducted to compare with $\alpha$-MG uptake. Treatment with cisplatin for 24 and 48 hours significantly increased activities of lactate dehydrogenase and $\gamma$-glutamyltransferase in culture medium at a concentration of 50$\mu$M. However, above 100$\mu$M of concentration, activities of these enzymes in media were dramatically decreased by cisplatin. These observations indicate that cisplatin has direct inhibitory effect on the activities of these enzymes and make it doutful to use enzyme leakage test to demonstrate damage of kidney cells by chemicals such as cisplatin over the appropriate range of concentration. Cisplatin inhibited $\alpha$-MG uptake at a low concentration which enzymes were not leaked. Also cadmium chloride and mercuric chloride which are acutely nephrotoxic in vivo, significantly inhibited $\alpha$-MG uptake at a low concentration. These results indicate that the uptake of $\alpha$-methylglucose in LLC-$PK_1$cell line is a useful biomarker for the study of nephrotoxicity.

• IMMUNE NETWORK
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• v.9 no.6
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• pp.248-254
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• 2009

[ $TGF-{\beta}1$ ]is well known to induce Ig germ-line ${\alpha}$ ($GL{\alpha}$) transcription and subsequent IgA isotype class switching recombination (CSR). Homeodomain protein TG-interacting factor (TGIF) and E3-ubiquitin ligases TGIF interacting ubiquitin ligase 1 (Tiul1) are implicated in the negative regulation of $TGF-{\beta}$ signaling. In the present study, we investigated the roles of Tiul1 and TGIF in $TGF{\beta}1$-induced IgA CSR. We found that over-expression of Tiul1 decreased $TGF{\beta}1$-induced $GL{\alpha}$ promoter activity and strengthened the inhibitory effect of Smad7 on the promoter activity. Likewise, overexpression of TGIF also diminished $GL{\alpha}$ promoter activity and further strengthened the inhibitory effect of Tiul1, suggesting that Tiul1 and TGIF can down-regulate $TGF{\beta}1$-induced $GL{\alpha}$ expression. In parallel, overexpression of Tiul1 decreased the expression of endogenous IgA CSR-predicitive transcripts ($GLT_{\alpha},\;PST_{\alpha},\;and\;CT_{\alpha}$) and $TGF{\beta}1$-induced IgA secretion, but not $GLT_{\gamma3}$ and IgG3 secretion. Here, over-expressed TGIF further strengthened the inhibitory effect of Tiul1. These results suggest that Tiul1 and TGIF act as negatively regulators in $TGF{\beta}1$-induced IgA isotype expression.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.485-493
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• 1997

We investigated the effect of ${\alpha}-adrenergic$ and cholinergic receptor agonists on $Ca^{2+}$ current in adult rat trigeminal ganglion neurons using whole-cell patch clamp methods. The application of acetylcholine, carbachol, and oxotremorine ($50\;{\mu}M\;each$) produced a rapid and reversible reduction of the $Ca^{2+}$ current by $17{\pm}6%,\;19{\pm}3%,\;and\;18{\pm}4%$, respectively. Atropine, a muscarinic antagonist, blocked carbachol- induced $Ca^{2+}$ current inhibition to $3{\pm}1%$. Norepinephrine ($50\;{\mu}M$) reduced $Ca^{2+}$ current by $18{\pm}2%$, while clonidine ($50\;{\mu}M$), an ${\alpha}2-adrenergic$ receptor agonist, inhibited $Ca^{2+}$ current by only $4{\pm}1%$. Yohimbine, an ${\alpha}2-adrenergic$ receptor antagonist, did not block the inhibitory effect of norepinephrine on $Ca^{2+}$ current, whereas prazosin, an ${\alpha}1-adrenergic$ receptor antagonist, attenuated the inhibitory effect of norepinephrine on $Ca^{2+}$ current to $6{\pm}1%$. This pharmacology contrasts with ${\alpha}2-adrenergic$ receptor modulation of $Ca^{2+}$ channels in rat sympathetic neurons, which is sensitive to clonidine and blocked by yohimbine. Our data suggest that the modulation of voltage dependent $Ca^{2+}$ channel by norepinephrine is mediated via an α1-adrenergic receptor. Pretreatment with pertussis toxin (250 ng/ml) for 16 h greatly reduced norepinephrine- and carbachol-induced $Ca^{2+}$ current inhibition from $17{\pm}3%\;and\;18{\pm}3%\;to\;2{\pm}1%\;and\;2{\pm}1%$, respectively. These results demonstrate that norepinephrine, through an ${\alpha}1-adrenergic$ receptor, and carbachol, through a muscarinic receptor, inhibit $Ca^{2+}$ currents in adult rat trigeminal ganglion neurons via pertussis toxin sensitive GTP-binding proteins.