• Korean journal of food and cookery science
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• v.14 no.4
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• pp.333-338
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• 1998

On the mutagenicity induced by 2-aminofluorene (2-AF) with S9 mix and N-Methyl-N＇-Nitro-N-Nitrosoguanidine (MNNG) without S9 mix, the antimutagenic effects of dietary fiber (total dietary fiber, u-cellulose and pectin) from Yam were examined by the Ames assay using Salmonella typhimurium TA98 and TA100. Total dietary fiber, $\alpha$-cellulose ind pectin from natural and cultural Yam didn＇t have mutagenicity. Most of sample dietary fiber showed the antimutagenicity. Total dietary fiber from cultural Yam was more effective than that from natural Yam on mutagenicity induced by 2-AF and MNNG. $\alpha$-cellulose from cultural Yam was more effective than that from natural Yam on mutagenicity caused by 2-AF and MNNG. Pectin from natural and cultural Yam had antimutagenic effect on mutagenicity induced by MNNG. In this study, antimutagenicity on MNNG was more effective than that on 2-AF. Antimutagenic effect of Samples had influence on incubation time. $\alpha$-cellulose and pectin from natural and cultural Yam showed stronger antimutagenic effect than standard $\alpha$-cellulose and standard pectin, respectively, on mutagenicity induced by 2-AF and MNNG.

• Applied Biological Chemistry
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• v.12
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• pp.25-31
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• 1969

The characteristics of crude enzyme produced from Trichoderma viride($O_2-1$) which isolated from half spoiled Locust acacia wood (Robinia Pseudacacia Linne) were examined in this paper. The results obtained were summarized as follows: 1) As a results of enzymatic action on several cellulose substrate it was found that there were some sorts of cellulase in crude enzyme. 2) The activity of C.M.C. ase and ${\beta}-glucosidase$ were decreased in accordance with increasing concentration of substrate, and filter paper saccharifying enzyme relatively increased in accordance with increasing concentration of substrate and enzyme in couse of time. 3) The optimal pH of each enzyme was 5.0 and the range of stability on pH generally from 3 to 6. 4) In disintegrating activity on filter paper, in decomposing activity on C.M.C. and $p-nitrophenyl-{\beta}-D-glucoside$, and in saccharifying activity on filter paper, the optimal temperatures were $50^{\circ}C.,\;60^{\circ}C,\;and\;65^{\circ}C$. 5) The order of stability on temperature was as follow; saccharifying activity on filter paper decomposing activity on C.M.C. disintegrating activity on filter paper>decomposing activity on $p-nitrophenyl-{\beta}-D-glucoside$. 6) The activity of the enzymes was inhibited with mercuric and silver ion, and activated with potassium.

• Journal of Physiology & Pathology in Korean Medicine
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• v.29 no.6
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• pp.492-497
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• 2015

In the present study, vasorelaxant effect of the extract of seeds of Oenothera odorata (SOO) and its possible mechanism responsible for this effect were examined in vascular tissues isolated from rats. Changes in vascular tension, 3',5'-cyclic monophosphate (cGMP) levels were measured in thoracic aorta rings from rats. Methanol extract of seeds of Oenothera odorata relaxed endothelium-intact thoracic aorta in a dose-dependent manner. A dose-dependent vascular relaxation was also revealed by treatment of ethylacetate, n-butanol, and H₂O (aqua extract of seeds of Oenothera odorata , ASOO) extracts partitioned from methanol, but not by hexane extract. However, the vascular relaxation induced by ASOO were abolished by removal of endothelium of aortic tissues. Pretreatment of the endothelium-intact vascular tissues with N^G-nitro-L-arginine methyl ester (L-NAME) or ¹H-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-1- one (ODQ) significantly inhibited vascular relaxation induced by ASOO. Moreover, incubation of endothelium-intact aortic rings with ASOO increased the production of cGMP. However, ASOO-induced increases in cGMP production were blocked by pretreatment with L-NAME or ODQ. The vasorelaxant effect of ASOO was attenuated by tetraethylammonium (TEA), 4-aminopyridine, and glibenclamide attenuated. On the other hand, the ASOO-induced vasorelaxation was not blocked by verapamil, and diltiazem. Taken together, the present study demonstrates that ASOO dilate vascular smooth muscle via endothelium-dependent NO-cGMP signaling pathway, which may be closely related with the function of K⁺ channels.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.2
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• pp.408-413
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• 2007

Vascular tone plays an important role in the regulation of blood pressure. In the present study, the methanol extract of Rosae multiflora Radix (MRM) induced dose-dependent relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pretreatment of the endothelium-intact aortic tissues with $N^G$-nitro-L-arginine methly ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-${\alpha}$]-quinoxalin-1-one (ODQ) inhibited the relaxation induced by MRM, respectively. But, the relaxation effect of MRM was not blocked by indomethacine, glibenclamide, tetraethylammonium (TEA), verapamil, diltiazem, atropine, and propranolol, respectively. Moreover, incubation of endothelium-intact aortic rings with MRM increased the production of cGMP. Taken together, the present results suggest that MRM relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling. These results would be useful for further study to MRM on animal models with cardiovascular diseases.

• Parasites, Hosts and Diseases
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• v.35 no.3
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• pp.189-196
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• 1997

The purpose of this study is to determine whether nitric oxide is involved in the extracellular killing of Trichomoncs uasinalis by mouse (BALB/c) peritoneal macrophages and RAW264.7 cells activated with LPS or rIFN-γ and also to observe the effects of various chemicals which affect the production of reactive nitrogen intermediates (RNl) in the cytotoxicity against T. vnginnlis. The cytotoxicity was measured by counting the release of (3H)-thymidine from labelled protozoa and NOa was assayed by Griess reaction. Nemonomethyl-L-arginine (L-NMHA), Nenitro-L-arginine methyl ester (NAME) and arginase inhibited cytotoxicity to T. vaginnlis and nitrite production by activated mouse perioneal macrophagrs and RAW 264.7 cells. The addition of excess L-arginine competitively restored trichomonacidal activity of macrophages. Exogenous addition of FeSO4 inhibited cytotoxicity to T. vaginaLis and nitric products of macrophages. From above results, it is assumed that nitric oxide plays an important role in the host defense mechanism of macrophages against T ucfinalis.

• Journal of Chest Surgery
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• v.29 no.5
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• pp.487-494
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• 1996

The neurogenic responses of tracheal smooth muscles to electrical field stimulation (EFS) is biphasic, consisting firstly of cholinergic contraction followed by a slow and sustained relaxation. It is well known that a sustained relaxation involves the inhibitory non-adrenergic non-cholinergic systems. This study was done to Investigate the relaxing agents and their action mechanisms by use of an organ bath with plati- ilum . The tracheal smooth muscle relaxation due to EFS was suppressed by L-NAME, the WO (Nitric Oxide) synthase inhibitor, and these effects were reversed by L-arginine, the precursor of NO. Also, L-WAME (HG-nitro-L-arginine methyl ester) increased the basal tension. Nitroprusside, the NO-donor, suppressed the tracheal basal tension greatly. Methylene blue, the inhibitor of guanylate cyclase, decreased EFS-induced relaxations and increa ed basal tension. Forskolin and isoprenaline, which are activators of adenylate cyclase, suppressed tracheal basal tension in the same way as nitroprusside. TEA (tetraethylammonium), the non-specific K'channel blocker, and apamin, the Ca"-activated K'channel blocker, increased tracheal basal tension and EFS-induced relaxations. Our results indicate that Pr3 Is released upon stimulation of the NANC (Won Adrenergic Won Cholinergic) nerves in guinea-pig tracheal smooth muscle and that the release of NO related with the K+ channel, as well as the release of other inhibitory agents< e. g.)VIP (Vasoactive Intestinal Polypeptide), PHI (Peptide Histidine Isoleusine) > mediated via CAMP (cyclic Adenosine Monophosphate) may be Involved In sustained relaxation.

• The Journal of Internal Korean Medicine
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• v.26 no.1
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• pp.182-198
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• 2005

Object : This study was designed to research whether the protection and inhibitory effects of cardiovascular diseases in L-NAME induced rat or ECV 304 cell lines through the Cell morphological pattern, Tunel assay, LDH activity, heart rate, blood pressure and immunohistochemistric analysis by Boonsimgieum water extract Methods : Nitric oxide(NO) play an important role in normal and pathophysiological cells including as a messenger molecule, neurotransmitter, microbiocidal agent, or dilator of blood vessels and artheriosclerosis, hypertension, myocardial infarction, respectively. Endothelial cell products can modulate the magnitude of a response to a vasoconstrictor, as evinced by the greater constriction after endothelium removal or NO synthesis blockade. To investigate that Boonsimgieum in the potential contribution of the levels of nitric oxide generated by endothelial nitric oxide synthase (eNOS) and the mechanisms of protection against NG-nitro-L-arginine methyl ester (L-NAME), human ECV 304 cells, which normally do not express eNOS, were expressed by L-NAME. L-NAME stimulated rat or cells were found to be resistant to injury and delayed death following the Boonsimgieum. Inhibition of nitric oxide synthesis abolished the protective effect against L-NAME, thrombin and collagen exposure. Interestingly, such effects have been observed during stimulation with agents such as phenylephrine and KCl on L-NAME mediate rats, were damaged by the NOS inhibitor L-NAME. Result : As the result of this study, In group, the anti-apoptosis and necrosis in the cardiovascular system have a potential capacity for prevented, protected and treating the diseases of cardiovascular system, against the necrosis of rat and ECV 304 cells with Caspase 3 and calpain expression by L-NAME is promoted. Conclusion : these results demonstrate neuroprotective and memory enhancing effects of ZIBU, suggesting its beneficial actions for the treatment of AD.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.521-527
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• 1998

An important property of the intestine is the ability to secrete fluid. The intestinal secretion is regulated by a number of substances including vasoactive intestinal peptide (VIP), ATP and different inflammatory mediators. One of the most important secretagogues is adenosine during inflammation. However, the controversy concerning the underlying mechanism of adenosine-stimulated $Cl^-$ secretion in intestinal epithelial cells still continues. To investigate the effect of adenosine on $Cl^-$ secretion and its underlying mechanism in the rabbit colon mucosa, we measured short circuit current ($I_{SC}$) under automatic voltage clamp with DVC-1000 in a modified Ussing chamber. Adenosine, when added to the basolateral side of the muocsa, increased $I_{SC}$ in a dose-dependent manner. The adenosine-stimulated $I_{SC}$ response was abolished when $Cl^-$ in the bath solution was replaced completely with gluconate. In addition, the $I_{SC}$ response was inhibited by a basolateral Na-K-Cl cotransporter blocker, bumetanide, and by apical $Cl^-$ channel blockers, dephenylamine-2-carboxylate (DPC), 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), glibenclamide. Amiloride, an epithelial $Na^+$ channel blocker, and 4,4-diisothiocyanato-stilbene-2,2-disulphonate (DIDS), a $Ca^{2+}-activated$ $Cl^-$ channel blocker, had no effect. In the mucosa pre-stimulated with forskolin, adenosine did not show any additive effect, whereas carbachol resulted in a synergistic potentiation of the $I_{SC}$ response. The adenosine response was inhibited by 10 ${\mu}M$ H-89, an inhibitor of protein kinase A. These results suggest that the adenosine-stimulated $I_{SC}$ response is mediated by basolateral to apical $Cl^-$ secretion through a cAMP-dependent $Cl^-$ channel. The rank order of potencies of adenosine receptor agonists was $5'-(N-ethylcarboxamino)adenosine(NECA)＞N^6-(R-phenylisopropyl)adenosine(R-$ PIA)＞2-[p-(2-carbonylethyl)-phenyl-ethylamino]-5'-N-ethylcarboxaminoadenosine(CGS21680). From the above results, it can be concluded that adenosine interacts with the $A_{2b}$ adenosine receptor in the rabbit colon mucosa and a cAMP-dependent signalling mechanism underlies the stimulation of $Cl^-$ secretion.

• Journal of the Korean Society of Food Science and Nutrition
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• v.37 no.6
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• pp.691-695
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• 2008

The study was carried out to evaluate the antimutagenic effects in methanol extracts of Korean soybean paste (doenjang) added with various kinds of water (germanium water, painted maple sap) or salt (sun-dried salt, roasted salt, one time bamboo roasted salt, nine times bamboo roasted salt). Methanol extracts of germanium water doenjang (Ge-D) and painted maple sap (Acer mono Max) doenjang (PM-D) exhibited significant inhibitory activity ($56{\sim}62%$) against aflatoxin $B_1$ ($AFB_1$) by adding of 1 mg/plate in Ames test. Also, methanol extracts of Ge-D and PM-D showed stronger antimutagenic activity toward N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in SOS chromotest than traditional doenjang (TD). Methanol extracts of doenjang made with four kinds of salt revealed antimutagenic activity toward MNNG; especially, doenjang extracts using one-time bamboo roasted salt (B1-D) showed 94% inhibition at the concentration of 5 mg/plate. Methanol extracts of B1-D also had the strongest inhibitory effect against MNNG of doenjang made with different salts in SOS chromotest. As the results indicate, the various kinds of water and salt have had separate effects on the antimutagenic activity of doenjang; therefore, further research on various physiological functions of water or salt added traditional doenjang is needed.

• Tuberculosis and Respiratory Diseases
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• v.53 no.2
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• pp.148-160
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• 2002

배 경 : 쥐를 고농도의 산소에 60시간 이상 노출시켰을 때 급성 폐손상이 유발되지만 내독소를 저용량으로 투여시에는 이러한 폐손상이 경감된다고 알려져 있으나 그 기전에 대하여는 확실히 밝혀지지 않고 있다. 산화질소(nitric oxide, NO)는 내독소나 염증성 사이토카인(cytokine) 등의 자극에 의해서 폐내 여러 염증세포에서 만들어지며 이 산화질소는 경우에 따라 우리 몸에 이롭거나 해로운 양면성을 지니고 있다. 저자들은 쥐에서 고농도의 산소에 의한 폐손상이 저농도의 내독소 투여로 경감되는 기전에, 산화질소가 중요한 역할을 하는지 또는 황산화효소나 다른 항염증성 사이토카인이 중요한 역할을 하는지를 규명하고자 하였다. 방 법 : 총 120마리의 쥐 (Sprague-Dawley rat)를 24마리씩 5군으로 나누어 대조군은 실내 공기를, 고농도 산소군은 100%의 산소를 100%의 산소를 60시간 투여하였고 내독소군은 100% 산소 투여시 2일간 저용량의 내독소를 투여하였다. 다른 두 군은 산화질소 합성 억제물인 aminoguanidine(AG)과 N-nitro-L-arginine methyl ester (L-NAME)를 각각 2일간 고농도 산소와 내독소에 더하여 투여하였다. 각각의 군에서 폐손상의 정도와 사망률을 관찰하고 superoxide dismutase(SOD), catalase, nitric oxide, IL-6, IL-11을 기관지폐포세척액에서 측정하고, 고농도산소 투여군의 폐조직에서 iNOS synthase rnRNA의 발현을 비교하였다. 결 과: 1. 100%의 산소에 60시간 노출시켰을 때 쥐의 사망률은 8.3% 이었고 내독소 투여군은 4.2%, NAME 투여군이 37.5%, AG 투여군이 25%로 산화질소 합성 억제제에 의하여 사망률의 증가가 관찰되었다. 2. 폐의 손상 정도를 나타내는 폐의 wet/dry 중량비와 늑막액도 100%의 산소에 노출된 군에서 증가되었고 내독소 투여에 의하여 감소되었으며 NAME나 AG 투여군에서는 오히려 증가되었다. 3. 이러한 내독소에 의한 폐손상 억제효과가 항산화효소인 SOD나 catalase, 또는 protective cytokine인 IL-6나 IL-11등의 증가와 관련이 있는지를 관찰하였으나 이들 모두에서 유의한 변화를 관찰하지 못하였다. 4. 산화질소는 100% 산소에 노출시킨 군에서도 증가하였으나 내독소 투여군에서 유의하게 더욱 증가하였고 이는 L-NAME 나 aminoguanidine의 투여시 감소하였다. 5. iNOS mRNA의 발현도 내독소 투여군에서 유의하게 증가하였다. 결 론 : 쥐의 고농소 산소 투여에 의한 폐손상은 저용량의 내독소 투여로 경감되며, 이는 주로 내독소 투여에 의한 iNOS mRNA의 발현을 유도하여 생성된 산화질소의 증가에 기인하는 것으로 생각된다.