• Journal of agriculture & life science
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• v.44 no.2
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• pp.57-66
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• 2010

The antioxidant and neuronal cell protective effects of water extract from purple sweet potato were investigated. The total phenolics and monomeric anthocyanin contents of purple sweet potato extract were 44.25 mg/g and 2,394 mg/L, respectively. The antioxidant activities of purple sweet potato extract were evaluated using various antioxidant tests, including 1,1-diphenyl- 2-picrylhydrazyl (DPPH), 2,2'-azino- bis-(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) radical scavenging activities, ferric reducing/antioxidant power (FRAP) and reducing power. In these assays, the extract of purple sweet potato presented significant radical scavenging activities, FRAP, and reducing power in a dose-dependent manner. MTT {3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyl- tetrazoliumbromide} reduction assay showed significantly increase in cell viability when PC12 cells were pretreated with purple sweet potato extract. Because oxidative stress is also known to increase neuronal cell membrane breakdown, we further investigated by lactate dehydrogenase (LDH) and neutral red uptake assay. Purple sweet potato extract inhibited oxidative stress-induced membrane damage in neuronal cells. Therefore, these data results demonstrated that water extract of purple sweet potato have antioxidant activity and neuronal cell protective effect thus it has great potential as a natural source for human health.

• 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.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.199-199
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• 1998

In this study, the effects of ursodeoxycholic acid (UDCA) on ischemia/reperfusion injury were investigated on retrograded aortic perfusion model. Hearts from Sprague-Dawley rats were perfused with oxygenated Krebs-Henseleit solution (pH 7.4, 37) on a Langendorff apparatus. After equilibration, hearts were treated with ursodeoxycholic acid 10, 20, 40 and 800 M or vehicle (0.04% DMSO) for 10 min before the onset of ischemia. Following 25 min of global ischemia, ischemic hearts were reperfused and allowed to recover for 30 min. The physiological (i.e. heart rate, left ventricular diastolic pressure, coronary flow and time to contracture formation) and biochemical (lactate dehydrogenase, LDH) endpoints were evaluated. In vehicle group, time to contracture formation (TTC) value was 19.5 min during ischemia, LVDP was 20.8 mmHg at the endpoint of reperfusion and LDH activity in reperfusate was 59.7 U/L. Cardioprotective effects of UDCA following ischemia/reperfusion consisted of a reduced TTC (EC$\_$25/ = 16.10 M), reduced LDH release and enhanced recovery of contractile function during reperfusion. Especially, the treatments of UDCA 80 M remarkably increased LVDP (68.1 mmHg) and reduced LDH release (33.2 U/L). Our findings suggest that UDCA ameliorates ischemia/reperfusion-induced myocardial damage, in agreement with physiological and biochemical parameters.

• Journal of Chest Surgery
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• v.24 no.7
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• pp.669-673
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• 1991

Fructose-l, 6-diphosphate as an additive to cold crystalloid cardioplegia [St. Thomas sol.] was studied prospectively in 60 patients undergoing open heart surgery from January 1, 1991, to June 30, 1991. Thirty patients received cardioplegia with FDP[group I ] and 30 patients received cardioplegia without FDP [group II ]. There were no differences between two groups pre-operatively with regard to age, heart disease, cross-clamp time, cardiac enzymes, or hemodynamic measurements [p>0.05]. Cardiopulmonary bypass was established using ascending aorta and vena cava cannulation employing moderate systemic hypothermia [30oC nasopharyngeal temperature] and hemodilution All patients received cardioplegia through the aortic root at aortic root pressure of 80mm Hg. The composition of the cardioplegic solution and its delivery were identical in both groups except for the addition of FDP[1.5 mg/mL] in group I. The cardioplegic infusate consisted of St. Thomas Hospital solution. The initial dose was infused through the aortic root. Topical myocardial cooling with saline slush was employed in all patients. Recorded operative data were cardiopulmonary bypass and cross-clamp times, amount of cardioplegic infusate. Blood samples for assessment of lactate dehydrogenase [LDH], creatine kinase [CK] and transaminases [GOT, GPT] were obtained before and at 1,2,3,7th postoperative period. Better myocardial protection effect was noted in group I than group II with respect to the % change of cardiac enzymes, although the differences were not significant. We conclude that FDP is a safe additive to crystalloid cardioplegia and may be beneficial in open heart surgery patients.

• Journal of the Korean Society of Physical Medicine
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• v.5 no.2
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• pp.265-272
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• 2010

Purpose : This study was investigated the effect of electroacupuncture stimulation on the change of blood biochemical components in the rat spinal cord injury(SCI) damaged by the 6-hydroxydopamine. Methods : SCI model rats were damaged in L1-L2 injected with 6-hydroxydopamine. The thirty Sprague-Dawley adult male rats were randomly divided into normal group, control group and electroacupuncture group. Experimental groups were applied as electroacupuncture(Es-160, ITO, Japan) for 15minutes during the low frequency(2 Hz) stimulation to zusanli. The enzyme concentration levels analysis of the hematological changes were measured of Glutamate Oxaloacetate Transaminase(GOT), Glutamate Pyruvate Transaminase(GPT), Lactate dehydrogenase(LDH) and motor function recovery change was evaluated by the rota-rod test. Results : This study were as follow : The concentration of GOT, LDH in experimental group was lower than control group(p<.05). The experimental group showed increase of motor function recovery more in compared to control group(p<.05). Conclusion : The results of this study showed that electroacupuncture to zusanli point have an effect on functional recovery after the 6-hydroxydopamine induced SCI in rats.

• Clinical and Experimental Pediatrics
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• v.55 no.7
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• pp.238-248
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• 2012

Purpose: Hypoxic-ischemic encephalopathy is an important cause of neonatal mortality, as this brain injury disrupts normal mitochondrial respiratory activity. Carnitine plays an essential role in mitochondrial fatty acid transport and modulates excess acyl coenzyme A levels. In this study, we investigated whether treatment of primary cultures of rat cortical neurons with L-carnitine was able to prevent neurotoxicity resulting from oxygen-glucose deprivation (OGD). Methods: Cortical neurons were prepared from Sprague-Dawley rat embryos. L-Carnitine was applied to cultures just prior to OGD and subsequent reoxygenation. The numbers of cells that stained with acridine orange (AO) and propidium iodide (PI) were counted, and lactate dehydrogenase (LDH) activity and reactive oxygen species (ROS) levels were measured. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and the terminal uridine deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling assay were performed to evaluate the effect of L-carnitine (1 ${\mu}M$, 10 ${\mu}M$, and 100 ${\mu}M$) on OGD-induced neurotoxicity. Results: Treatment of primary cultures of rat cortical neurons with L-carnitine significantly reduced cell necrosis and prevented apoptosis after OGD. L-Carnitine application significantly reduced the number of cells that died, as assessed by the PI/AO ratio, and also reduced ROS release in the OGD groups treated with 10 ${\mu}M$ and 100 ${\mu}M$ of L-carnitine compared with the untreated OGD group (P<0.05). The application of L-carnitine at 100 ${\mu}M$ significantly decreased cytotoxicity, LDH release, and inhibited apoptosis compared to the untreated OGD group (P<0.05). Conclusion: L-Carnitine has neuroprotective benefits against OGD in rat primary cortical neurons in vitro.

• Korean Journal of Agricultural Science
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• v.47 no.3
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• pp.497-508
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• 2020

In this study, we investigated the protective effects of 'Donganme' (Sorghum bicolor L. Moench) against oxidative stress under in vitro conditions and in a cellular system using C6 glial cells. The radical scavenging activities were observed using the substrates 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl (•OH) radicals. The Donganme extract had an •OH radical scavenging activity of 82.66% at a concentration of 100 ㎍·mL^-1. Additionally, when DPPH was used as the substrate, the Donganme extract exhibited a strong radical scavenging activity in a concentration-dependent manner with an IC₅₀ value of 28.56 ㎍·mL^-1. Furthermore, treating C6 glial cells with hydrogen peroxide (H₂O₂) reduced the cell viability and generated reactive of oxygen species (ROS) and lactate dehydrogenase (LDH) compared to the normal levels, indicating that H₂O₂ induced oxidative stress. However, Donganme extracts increased the cell viability and inhibited ROS and LDH production against oxidative stress by H₂O₂ in the C6 glial cells. In particular, it showed effective cell protection with the cell viability, ROS production, and LDH release at 83.50, 88.06, and 14.87%, respectively, which were lower than the control or similar to the normal levels even at a low concentration of 100 ㎍·mL^-1. The present study suggests that the Donganme extract was effective in protecting against oxidative stress in C6 glial cells through its antioxidant activity. Thus, Donganme could be a promising therapeutic agent for neurodegenerative diseases due to oxidative stress.

• Korean Journal of Clinical Laboratory Science
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• v.43 no.2
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• pp.75-81
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• 2011

To clarify the oxidative stress of reactive oxygen species (ROS) and the effect of Chrysanthemum morifolium L. (CM) flower extract on the cultured neuroglial cells (C6 glioma) damaged by ROS, cell adhesion effect was measured by colorimetric assay after cultured C6 glioma cells were treated with various concentrations of glucose oxidase (GO) for 5 hours. For the antioxidative effect of CM flower extract, cell adhesion activity (CAA), superoxide dismutase (SOD)-like activity and lactate dehydrogenase (LDH) activity were assessed against GO-induced cytotoxicity on same cultures. In this study, GO remarkably decreased CAA dose-dependently, and the $XTT_{90}$ and $XTT_{50}$ values were measured at 15 mU/mL and 50 mU/mL following the treatment of C6 glioma cells with 5~60 mU/mL of GO. The CM flower extract significantly increased cell adhesion activity damaged by GO-induced cytotoxicity, and it also showed the SOD-like activity and the decrease of LDH activity. From these results, it is suggested that GO was cytotoxic on cultured C6 glioma cells, and CM flower extract showed antioxidative effects as shown by the increased CAA, SOD-like activity and the decrease of LDH activity on GO-induced cytotoxicity on the same cultures.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.4
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• pp.357-363
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• 2015

The purpose of this study was to compare the inhibitory effect of bevacizumab on human Tenon's fibroblasts (HTFs) cultured from primary and recurrent pterygium. Cultured HTFs were exposed to 2.0, 5.0, 7.5, and 15.0 mg/mL concentration of bevacizumab for 24 hours. The 3-[4,5-dimethylthiazol- 2-yl]-2,5-diphenyl tetrazolium bromide and lactate dehydrogenase leakage assays were then performed to assess fibroblast metabolism and viability. The matrix metalloproteinase (MMP), procollagen type I C terminal propeptide (PIP), and laminin immunoassays were performed to examine extracellular matrix production. Changes in cellular morphology were examined by phase-contrast and transmission electron microscopy. Both metabolic activity and viability of primary and recurrent pterygium HTFs were inhibited by bevacizumab in a dose-dependent manner, especially at concentrations greater than 7.5 mg/mL. Both types of HTFs had significant decreases in MMP-1, PIP, and laminin levels. Distinctly, the inhibitory effect of bevacizumab on MMP-1 level related with collagenase in primary pterygium HTFs was significantly higher than that of recurrent pterygium. Significant changes in cellular density and morphology both occurred at bevacizumab concentrations greater than 7.5 mg/mL. Only primary pterygium HTFs had a reduction in cellular density at a bevacizumab concentration of 5.0 mg/mL. Bevacizumab inhibits primary and recurrent pterygium HTFs in a dose-dependent manner, especially at concentrations greater than 7.5 mg/mL. As the primary HTFs produces larger amounts of MMP-1 compared to recurrent HTFs, significant reduction in MMP-1 level in primary pterygium HTFs after exposure to bevacizumab is likely to be related to the faster cellular density changes in primary pterygium HTFs.