• Journal of Food Hygiene and Safety
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• v.8 no.3
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• pp.157-161
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• 1993

In order to get infonnations on the development of alcohol induced cardiovascular disorders, primary cultured vascular smooth muscle cells (PVSMC) were treated with acetaldehyde, one of the most reactive metabolites of ethanol. Acetaldehyde caused the striking release of lactate dehydrogenase (LDH) from PVSMC and it stimulated the prostaglandin synthesis in the same system. But it didn't induce cyclooxygenase activity. lipoxygenase inhibitors-propyl gallate and nordihydroguaiaretic acid could reverse the effect of acetaldehyde, but dexamethasone, a phospholipase $A_2\;(PIA_2)$ inhibitor and cyclooxygenase inhibitors except indomethacin could not protect the cells from acetaldehyde toxicity. These results indicate that enhanced prostaglandin synthesis by acetaldehyde is not a direct cause of cell death, but secondary effect due to the activation of PIAl and also, the roles of the lipoxygenase metabolites and/or $PIA_2$ activity itself might be more important in the cytotoxicity of acetaldehyde.

• Journal of Acupuncture Research
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• v.22 no.5
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• pp.151-160
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• 2005

Objectives : This study was undertaken to examine whether Juglandis Semen herbal acupuncture (JGA) exerts protective effect against oxidant-induced cell injury in rabbit liver. Methods : The cell damage was estimated by measuring lactate dehydrogenase (LDH) release, and lipid peroxidation was estimated by measuring malondialdehyde (MDA) in rabbit liver slices. Results : t-Butylhydroperoxide (tBHP) caused an increase in LDH release and lipid peroxidation in a dose-dependent manner over concentrations of 0.5-2 mM, which were prevented by addition of 0.05% JGA. The protective effect of JGA was dose-dependent in concentration range of 0.005 to 0.1%. The concentrations of 0.005 and 0.1% JGA completely prevented the LDH release and lipid peroxidation by 1 mM tBHP. When liver tissues were exposed to 1 mM tBHP, alanine aminotransferase (ALT) activity in the medium was significantly increased, which was prevented by 0.05% JGA. tBHP (2 mM) decreased GSH content and the effect was prevented by 0.05% JGA. Conclusion : These results suggest that JGA exerts protective effect against oxidant-induced cell injury by antioxidant action resulting from enhancement of GSH content in the liver.

• Preventive Nutrition and Food Science
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• v.20 no.1
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• pp.73-77
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• 2015

As an approach to search for chemopreventive agents, we tested p-coumaric acid, 3-methoxy-p-coumaric acid (ferulic acid), and 3,5-dimethoxy-p-coumaric acid (sinapic acid) in B16/F10 melanoma cells. Intracellular melanin contents were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and cytotoxicity of the compounds were examined by lactate dehydrogenase (LDH) release. p-Coumaric acid showed inhibitory effect on melanogenesis, but ferulic acid increased melanin content, and sinapic acid had almost no effect on melanogenesis. Treatment with ferulic acid resulted in a 2 to 3 fold elevation in the production of melanin. Correlatively, cell viability decreased in a dose-dependent manner when treated with ferulic acid. However, ferulic acid did not affect the LDH release from the cells. Treatment with sinapic acid resulted in a 50~60% elevation in the release of LDH when treated with a $200{\mu}g/mL$ concentration and showed neither cytostasis nor increase of melanin synthesis in a dose-dependent manner. Taken together, p-coumaric acid inhibits melanogenesis, ferulic acid induces melanogenesis, and sinapic acid exerts cytotoxic effects in B16/F10 murine melanoma cells. The results indicate that the addition of methoxy groups to p-coumaric acid shows the melanogenic or cytotoxic effects in melanoma cells compared to the original compound. Therefore, this study suggests the possibility that methoxylated p-coumaric acid, ferulic acid can be used as a chemopreventive agent.

• Journal of Applied Biological Chemistry
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• v.64 no.2
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• pp.105-112
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• 2021

Excessive accumulation of the amyloid beta (Aβ) peptide has been implicated in the pathogenesis of Alzheimer's disease (AD). Paeonia lactiflora (PL) has been used in treatments of several conditions such as inflammation, arthritis, and cognitive impairment. The purpose of this study was to investigate the neuroprotective effect and mechanisms of PL and its active compound, paeoniflorin (PF), on Aβ_25-35-induced neurotoxicity in SH-SY5Y cells. We evaluated cell viability, lactate dehydrogenase (LDH) release and reactive oxygen species (ROS) production. Furthermore, underlying mechanism of PL and PF on the regulation of amyloidogenic pathway was analyzed by Western blotting. In our results, Aβ_25-35-induced neuronal cell loss was observed, whereas treatment with PL (10, 50, and 100 ㎍/mL) and PF (1, 5, and 10 ㎍/mL) significantly elevated the cell viability, and decreased LDH release and ROS production. In addition, exposure of SH-SY5Y cells to Aβ_25-35 significantly increased the protein levels of amyloid precursor protein (APP)-C-terminal fragment β, β-site APP-cleaving enzyme, and presenilin-1 and -2. However, treatment with PL and PF inhibited the amyloidogenic pathway via the down-regulation of those protein expressions. Taken together, our results indicate that PL, and its active compound PF, could protect SH-SY5Y cells against Aβ_25-35-induced cell neurotoxicity by attenuating LDH release and ROS production, and these effects may be attributed to regulation of amyloidogenic pathway-related protein expression. In conclusion, PL and PF could be a potential to prevent neurodegenerative disorders such as AD.

• Journal of Life Science
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• v.20 no.11
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• pp.1595-1602
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• 2010

Oxidation of low density lipoprotein (LDL) has been recognized as an important role in the initiation and progression of atherosclerosis. In this study, effects of allylmercaptan, a major metabolite compound of garlic, was studied on endothelial cell injury induced by oxidized low density lipoprotein (ox-LDL). The antioxidative activity of allylmercaptan was investigated by monitoring a thiobarbituric acid substance (TBARS). Allylmercaptan inhibited LDL oxidation induced by $Cu^{2+}$ at concentrations of 0.1, 1 and 10 mM in a dose dependent manner. Lactate dehydrogenase (LDH) release, as an index of cell injury, and intracellular glutathione levels were determined. Pulmonary artery endothelial cells were preincubated with allylmercaptan at $37^{\circ}C$ and 5% $CO_2$ for 24 hr, washed, and then exposed to 0.1 mg/ml oxidized LDL for 24 hr. Preincubation of endothelial cells with allylmercaptan significantly prevented the LDH release and depletion of GSH. Peroxides were measured directly in 24 well plates using a fluorometric assay. Allylmercaptan inhibited release of peroxides induced by ox-LDL in pulmonary artery endothelial cells. In a free system, allylmercaptan was shown to scavenge hydrogen peroxide. The data indicate that allylmercaptan can protect pulmonary artery endothelial cells from injury caused by oxidized LDL, and suggest that allylmercaptan may be useful for the prevention of atherosclerosis.

• Korean Journal of Pharmacognosy
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• v.26 no.1
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• pp.51-56
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• 1995

To devise an in vitro screening method for antihepatotoxic activity, $CCl_4-induced$ cytotoxicities in primary cultures rat hepatocytes were examined. When rat hepatocytes were intoxicated with 0.5, 1.0 or 1.5 mM $CCl_4$ for 1.5, 3 or 19hr, in order of LDH>GOT>GPT release form hepatocytes was increased in a dose-dependent manner. Treatment with 1.5 mM $CCl_4$ for 1.5 hr showed maximum increase in activity of LDH, GOT or GPT released in the medium compared with the control. At this experimental condition, well known antihepatotoxic substances, glycyrrhizin and silybin markedly inhibited $CCl_4-induced$ cytotoxicities. These results demonstrated that the screening method using $CCl_4-induced$ injury in primary cultured rat hepatocytes might be suitable in vitro assay for antihepatotoxic activity.

• 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.

• Restorative Dentistry and Endodontics
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• v.21 no.1
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• pp.403-424
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• 1996

Cell culture methods have been used to assess the cytotoxicity of dental materials. Different paramaters are used to monitor cytotoxic effects. But it is difficult to compare each investigator's results with different methods. The objective of this study was to investigate cytotoxic effect of several retrograde filling materials according to cell lines and assay methods. Cytotoxicity of Bestalloy (Dogmyung, Korea), Prisma APH(Densply International Inc., U.S.A.), Clearfil FII (Kuraray Co., Japan), Fuji II (GC Co., Japan), Fuji II LC (GC Co., Japan) and IRM (Densply Co., U.S.A.) on L929, 3T3 and KB permanent cell lines was measured. Radiochromium, Lactate dehydrogenase (LDH) release method and colorimetric assays, namely neutral red (NR) and MTT were used. Each material was mixed according to the manufacturer's instruction. They were tested as solid and extracted state. Cell culture media were added to each mixed or solid materials then the solution was collected and used as extract solutions. Solid Fuji II showed mild cytotoxicity on three cell lines using radiochromium release method. There was no difference in cytotoxicity of extract solution group using radiochromium release method. In colorimetric assay immediate Fuji II group and all the IRM groups showed severe cytotoxic effect. Difference in cyctotoxicity was due to rather kinds of cell lines than assay methods. Solid Fuji II and IRM showed mild cytotoxicity on three cell lines. But extract solutions had different cytotoxic effect according to cell lines using LDH release assay. Light-cured glass ionomer had mild to moderate degree of cytotoxicity on three cell lines. Cytotoxicity was affected by specimen prepaton. Susceptibility of each cell ines were also affected by assay emthods. It was suggested that cytotoxicity study using only one cell line and/or assay method might not accurately reflect the real toxic nature of dental biomaterials.

• Journal of Life Science
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• v.30 no.7
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• pp.598-605
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• 2020

Padina gymnospora is a brown algae of the class Phaeophyceae. It has been established that P. gymnospora ameliorates amyloid-β-induced neuropathology and has an anticoagulation effect, but this study was designed to estimate its skin-whitening effect and identify its active component. The ingredients of P. gymnospora were extracted with ethanol and its activity was compared with arbutin. First, the P. gymnospora extract was observed to inhibit tyrosinase activity in a dose-dependent manner, tyrosinase being the rate-limiting enzyme of melanin synthesis. Notably, where 200 μM of arbutin inhibited tyrosinase activity by 58.1%, P. gymnospora extract (0.5%) achieved 76.7%. The P. gymnospora extract also significantly reduced α-melanocyte-stimulating hormone-induced TRP-1 and TRP-2 mRNA expression. In addition, it significantly inhibited melanin synthesis in B16F10 melanoma cells. We identified the 0.66% fucosterol content that inhibited melanin synthesis as comparable to that of arbutin. Additionally, we tested the potential cytotoxicity of P. gymnospora by MTT and LDH release assay and found that the extract significantly reduced LDH release in CCD-986sk cells. These results indicate that P. gymnospora extract could be a potential active ingredient of cosmetics with a skin-whitening effect.

• Journal of Acupuncture Research
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• v.18 no.4
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• pp.143-151
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• 2001

Objective : This study was undertaken to determine whether Scutellaria balicalensis Georgi (SbG) extract exerts the protective effect against oxidant-induced alterations in organic cation transport in the renal proximal tubule. Methods : Organic cation transport was estimated by examining alterations in tetraethylammon - ium(TEA) uptake in rabbit renal cortical slices. The slices were treated with 0.2 mM tBHP for 60 min at $37^{\circ}C$. tBHP caused an inhibition in TEA uptake by renal cortical slices. Such an effect was accompanied by depressed Na+-K+-ATPase activity and ATP depletion. tBHP also induced a significant increase in LDH release. Results : SbG prevented tBHP-induced inhibition of TEA uptake in a dose-dependent manner at the concentration ranges of 0.05-0.1%. tBHP-induced inhibition of Na+-K+-ATPase activity and ATP depletion were significantly prevented by 0.05% SbG. tBHP-induced LDH release also was blocked by SbG. tBHP caused a significant increase in lipid peroxidation and its effect was prevented by SbG. Conclusion : These results suggest that SbG prevents oxidant-induced alterations in organic cation transport in rabbit renal cortical slices. Such protective effects of SbG may be attributed to inhibition of peroxidation of membrane lipid.