• Journal of dental hygiene science
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• v.2 no.1
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• pp.25-29
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• 2002

In the present study, we tried to investigate whether poly-L-lysine(PLL)(MW 78,000 and 9,600) significantly affect mucin release from cultured hamster airway goblet cells. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled with $^3H$-glucosamine for 24 hr and chased for 30 min in the presence of varying concentrations of PLL to assess the effects on $^3H$-mucin release. Possible cytotoxicities of PLL were assessed by measuring Lactate Dehydrogenase(LDH) release during treatment. The results were as follows : (1) PLL significantly inhibited mucin release from cultured HTSE cells in a dose-dependent manner; (2) there was no significant release of LDH by treatment of PLL 9,600; (3) however, in the case of treatment of PLL 78,000, there was significant release of LDH during treatment. We conclude that PLL which has molecular weight under 10,000 might inhibit mucin release from airway goblet cells without significant cytotoxicity. This finding suggests that PLL might be used as a tool of research for the hypersecretion of airway mucus.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.6
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• pp.1409-1415
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• 2009

Obesity is especially a serious health problem in industrialized countries, because it is considered to be a risk factor associated with the genesis or development of various metabolic diseases, including cardiovascular disease and type 2 diabetes mellitus. The purpose of this study was to investigate the effects of tanshinone IIA from Salvia miltiorrhiza Bunge on induction of apoptossis and inhibition of adipogenesis in in 3T3-L1 preadipocytes and adipocytes. The results demonstrated that tanshinone IIA decreased cell population growth of 3T3-L1 preadipocytes, assessed with the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] and LDH (lactate dehydrogenase) assay. Flow cytometric analysis of 3T3-L1 preadipocytes exposed to tanshinone IIA showed that apoptotic cells increased in a timeand dose-dependent manner. Treatment with tanshinone IIA decreased the number of normal cells and increased the number of apoptotic cells in a dose-dependent manner. The induction of apoptosis in 3T3-L1 preadipocytes by tanshinone IIA was mediated through the activation of caspase-3 and Bax, and then through the cleavage of PARP and the down-regulation of Bcl-2. Moreover, tanshinone IIA significantly decreased the amount of intracellular triglycerides and GPDH (glycerol-3-phosphate dehydrogenase) activity in 3T3-L1 adipocytes. Our results suggest that tanshinone IIA efficiently induces apoptosis and inhibits adipogenesis in 3T3-L1 preadipocytes and adipocytes.

• Proceedings of the Ginseng society Conference
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• 2002.10a
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• pp.545-555
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• 2002

Ginsenosides of 20(S)-protopanaxadiol and 20(S)-protopanaxatriol classification including the aglycones, PD, PI and ginsenosides Rh2, Rhl were shown to posses characteristic effects on proliferation of THP-l human leukaemia cells. A similar result was not apparent for ginsenoside Rg3 or dexamathasone. The concentration to inhibit $50\%$ of cells $(LC_{50})$ for PD, Rh2, PI and Rhl were 13 ${\mu}g/mL,\;15{\mu}g/mL,\;19{\mu}g/mL\;and\;210\;{\mu}g/mL$ respectively. Cell cycle analysis showed apoptosis with PD and PI treatment of THP-1 cells resulting in a build up of sub-G1 cells after 24, 48 and 72 hours of treatment. Rh2, and dexamathasone treatments also increased apoptotic cells after 24 hours, where as Rhl did not. After 48 and 72 hours Rh2, Rhl and dexamathasone similarly increased apoptosis, but these effects were significantly (P<0.05) lower than observed for both PD and PI treatments. Furthermore, treatments that produced the largest build up of apoptotic cells were also found to have the largest release of lactate dehydrogenase (LDH). It can be concluded from these studies that the presence of sugars to PD and PI aglycone structure reduces the potency to induce apoptosis, and alternately alter membrane integrity. These cytotoxic effects to THP-l cells were different from dexamethasone.

• Biomolecules & Therapeutics
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• v.7 no.4
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• pp.354-361
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• 1999

In this study, the effects of tauroursodeoxycholic acid (TUDCA) on ischemia/ reperfusion injury were investigated on isolated heart perfusion models. Hezrts were perfused with oxygenated Krebs-henseleit solution (pH 7.4, $37^{\cire}C$) on a Langendorff apparatus. After equilibration, isolated hearts were treated with TUDCA 100 and 200 $\mu\textrm{M}$ or vehicle (0.02% DMSO) for 10 min before the onset of ischemia in single treatment group. In 7 day pretreatment group. TUDCA 50, 100 and 200 mg/kg body weight were given orally for 7 days before operation. After global ischemia (30 min), ischemic hearts were reperfused for 30 min. The physiological (i.e. heart rate, left ventricdular developed pressure, coronary flow, double product, time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 810 sec during ischemia, LVDP was 34.0 mmHg at the endpoint of reperfusion and LDH activity in total reperfusion effluent was 34.3 U/L. Single treatment with TUDCA did not change the postischemic recovery of cardiac function, LDH and time to contractur compared with ischemic control group. TUDCA pretreatment showed the tendency to decrease LDH release and to increase time to contracture and coronary flow. Our findings suggest that TUDCA does not ameliorate ischemia/reperfusion-reduced myocardial damage.

• Archives of Pharmacal Research
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• v.22 no.5
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• pp.479-484
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• 1999

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on isolated heart perfusion model. Hearts were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, $37^{\circ}C$) on a Langendroff apparatus. After equilibration, isolated hearts were treated with UDCA 20 to 160 $\mu$M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. After global ischemia (30 min), ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular developed pressure, coronary flow, double product and time to contracture formation) and biochemical (lactate dehydrogenase; LDH) parameters were evaluated. In vehicle-treated group, time to contracture formation was 21.4 min during ischemia, LVDP was 18.5 mmHg at the endpoint or reperfusion and LDH activity in total reperfusion effluent was 54.0 U/L. Cardioprotective effects of UDCA against ischemia/reperfusion consisted of a reduced TTC $(EC_{25}=97.3{\mu}M)$, reduced LDH release and enhanced recovery of cardiac contractile function during reperfusion. Especially, the treatments of UDCA 80 and $160 {\mu}M $ significantly increased LVDP and reduced LDH release. Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage.

• Natural Product Sciences
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• v.18 no.2
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• pp.76-82
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• 2012

Stamens of Mesua ferrea L. are a well-known herbal drug used in Indian System of Traditional Medicine to treat various diseases. The claimed activity of this plant part is necessitated to investigate antioxidant and hepatoprotective activity. Authenticated plant sample was extracted with hexane, ethanol (EtOH) and water (aq.) using ASE 100 accelerated solvent extractor. Antioxidant activity was evaluated by means of different in vitro assays. Hepatoprotective effect was investigated on carbon tetrachloride induced oxidative stress in liver slice culture model. Cytotoxic marker lactate dehydrogenase (LDH) released in culture medium and the activity of lipid peroxidation along with antioxidant enzymes (AOEs) namely superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) were estimated. Hexane and EtOH extracts were significantly inhibited DPPH, NO, SOD and $ABTS^+$ radical in dose dependent manner. The trade of phenol content was: aq. extract < hexane extract < EtOH extract. A significant correlation was shown by total phenol content and free radical scavenging activity of extracts. The culture system treated with hexane extract, EtOH extract or ascorbic acid exhibited significant depletion in LDH, lipid peroxidation, antioxidative enzymes SOD, CAT and GR. Hexane extract and EtOH extracts of stamen of M. ferrea protected liver slice culture cells by alleviating oxidative stress induced damage to liver cells.

• Korean Journal of Agricultural Science
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• v.44 no.4
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• pp.586-594
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• 2017

Mitochondrial activity affects skeletal muscle energy metabolism and phenotype. To address whether mitochondrial activity can modulate muscle phenotype in vitro, protein expression of myosin heavy chain (MyHC) in C2C12 muscle cell lines was investigated after treated with antimycin A, an inhibitor of oxidative phosphorylation in mitochondria. Fully differentiated C2C12 myotubes were administrated with different concentration of antimycin A including 0, 100, 200, 500, 700, and 1000 ng/mL. After 72 h treatment, myosin heavy chain isoform expression and related enzyme activity (lactate dehydrogenase; LDH and creatine kinase) were analyzed. Administration of antimycin A changed expression of MyHC in C2C12 myotubes showing a shift from slow to fast twitching muscle type. Protein expression of MyHC type 2b (fast twitching muscle type) was decreased (P < 0.05) by antimycin A treatment (500, 700, and 1000 ng/mL) when compared with control group. Administration of antimycin A (1000 ng/mL), however, decreased (P < 0.05) MyHC type I (slow twitching muscle type). Interestingly, LDH activity was increased (P < 0.05) by antimycin A treatment. Results from our current study proposed a possibility that skeletal muscle phenotype, including MyHC and LDH activity, can be shifted from slow to fast twitching type by inhibiting the mitochondrial activity in C2C12 myotubes.

• Journal of the Korean Applied Science and Technology
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• v.39 no.6
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• pp.760-768
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• 2022

The purpose this study was to investigate the influences of 5% mung bean (Phaseolus aureus L.) on BUN and enzyme activities in serum of hyperlipidemic rats. Sprague-Dawley(SD) rats (24 male) were divided into four groups, namely the BD group(normal-nonhyperlipidemic diet), BM group(normal-nonhyperlipidemic diet+5% mung bean), BH group(control-hyperlipidemic diet), and BHM group(hyperlipidemic diet+5% mung bean). Serum concentrations of blood urea nitrogen (BUN) and uric acid were significantly decreased (p<0.05) by mung bean supplementation diet. The activities of AST, ALT, ALP, LDH, amylase and lipase in sera of mung bean diet group were significantly decreased (p<0.05). The catalase activity in serum of mung bean supplementation group was significantly increased than hyperlipidemic diet (p<0.05). In vivo experiment with hyperlipidemic rats showed that ingestion of mung bean were effective in kidney and hepatic functional enzyme activities. Which suggests that mung bean material could be used for further studies as a potential source for nutraceutical foods.

• Journal of Environmental Science International
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• v.29 no.4
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• pp.351-359
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• 2020

The purpose of this study was to investigate the improvement effect of mung bean (Phaseolus aureus L.) on the hepatic functional enzyme and catalase activity of streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley (SD) male rats were divided into four groups (n=6), and fed experimental diets containing mung bean meal [basal diet+5% mung bean (BM), basal diet+STZ+5% mung bean (SM)], and control (Basal Diet, BD), BS groups (basal diet+STZ). Serum concentrations of Blood Urea Nitrogen (BUN) and creatinine were significantly decreased (p<0.05) by 5% mung bean supplementation diet. The activities of aspartate transaminase (AST), alanine transaminase (ALT), akaline phosphatase (ALP), lactate dehydrogenase (LDH), amylase and lipase were decreased in the BD, BM and SM group than BS group. The catalase (CAT) activity was significantly increased (p<0.05) in mung bean supplementation diet (BM, SM group) than diabetic group (BS). In vivo experiments with diabetic rats showed that ingestion of mung bean supplementation diet were effective in BUN concentration, and hepatic functional enzyme activities.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.3
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• pp.1125-1131
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• 2014

Background: Schistosomiasis is a parasitic disease causing chronic ill health in humans with a serious consequences for socio-economic development in tropical and subtropical regions. There is also evidence linking Schistosoma mansoni to colonic carcinoma occurrence. The aim of this study was to evaluate some inflammatory and oxidative stress biomarkers, as well as L-fucose as linkers between intestinal schistosomiasis and colonic dysplasia development in mice. Materials and Methods: This study was conducted upon 80 mice that were divided the control group (10 non infected mice) and infected group which was subdivided into 7 sub-groups (10 mice each) according to the time of sacrifaction in the post infection (p.i.) period, 10 mice being sacrificed every two weeks from 6 weeks p.i. to 18 weeks p.i. Tumor necrosis factor alpha (TNF-${\alpha}$), inducible nitric oxide synthase (iNOS), and pentraxin 3 (PTX3) levels were estimated by immunoassay. The L-fucose level, and thioredoxin reductase (TrxR) and lactate dehydrogenase (LDH) activities were also evaluated in colonic tissue. Results: The current study revealed statistically significant elevation in the studied biochemical markers especially at 16 and 18 weeks p.i. The results were confirmed by histopathological examination that revealed atypical architectural and cytological changes in the form of epithelial surface serration and nuclear hyper-chromatizia at 14, 16 and 18 weeks p.i. Conclusions: inflammation, oxidative stress and L-fucose together may form an important link between Schistosomal mansoni infection and colonic dysplasia and they can be new tools for prediction of colonic dysplasia development in experimental schistosomiasis.