• Korean Journal of Environmental Agriculture
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• 제5권2호
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• pp.149-155
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• 1986

The fatty acid compositions of phospholipids extracted from leaves and leaf mitochondria, which were sampled from several horicultural plants grown under blue color-deficient sunlight (BCDS), were determined and compared with those from plants grown under natural white colored sunlight(WCS). It was found that the mitochondria isolated from plants grown under BCDS contained phospholipid whose degree of unsaturation in unit of number of double bonds per lipid molecule was remarkably higher than that from plants grown under WCS, the relative increment being $8{\sim}49%$. This was significantly larger than the relative increment, $4{\sim}8%$ for total phospholipid extracted from whole leaves grown under BCDS campared to WCS. This observation demonstrated that the blue light effect of sunlight on the chemical property of cellular membranes, as long as it was concerned with fatty acid composition, arose mainly at the mitochondrial membrane. Also observing that the degree of unsaturation of mitochondrial phospholipid was much lower than that of total phospholipid, it was interpreted that this was the consequence of rather active oxidative destruction of lipid-fatty acid components occuring in mitochondrial membrane by the reactive oxygen species, especially superoxide($O_2-$), which was known to be produced in mitochondrial inner membrane through the side reactions of the respiratory electron transport chain and also probably through the photosensitized reaction involving oxygen induced by blue colored light. Thus, it may be tentatively concluded that the extent of photosensitization in mitochondrial membrane could be considerably reduced under BCDS resulting in lowering of the $O_2-$ level in the respirating organelle The possible involvement of photodynamic action in membrane oxidation was also indicated by the fact that the typical fat-soluble antioxidant, ${\alpha}-tocopherol$, was found to be contained on a higher level in leaves under BCDS than those under WCS.

• The Korean Journal of Physiology and Pharmacology
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• 제1권1호
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• pp.1-12
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• 1997

As it has been reported that the depolarization induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1$ adenosine heteroreceptor and various evidence suggest that indicate the $A_2$ adenosine receptor is present in the striatum, this study was undertaken to delineate the role of adenosine receptors on the striatal ACh release. Slices from the rat striatum were equilibrated with $[^3H]$choline and then the release amount of the labelled product, $[^3H]$ACh, which was evoked by electrical stimulation (rectangular pulses, 3 Hz, 2 ms, 24 mA, $5\;Vcm^{-1}$, 2 min), was measured, and the influence of various agents on the evoked tritium outflow was investigated. And also, quantitative receptor autoradiography and drug-receptor binding assay were performed in order to confirm the presence and characteristics of $A_1$ and $A_2$ adenosine receptors in the rat striatum. Adenosine $(10{sim}100\;{mu}M)$ and $N^6$-cyclopentyladenosine (CPA, $1{sim}100\;{mu}M)$ decreased the $[^3H]$ACh release in a dose-dependent manner without changing the basal rate of release in the rat striatum. The reducing effects of ACh release by adenosine and CPA were abolished by 8-cyclopentyl-1,3-dipropy-Ixanthine (DPCPX, 2 ${mu}M$), a selective $A_1$, adenosine receptor antagonist, treatment. The effect of adenosine was potentiated markedly by 3,7-dimethyl-1-propargylxanthine (DMPX, 10 ${mu}M$), a specific $A_2$ adenosine receptor antagonist. 2-P-(2-carboxyethyl)phenethylamimo-5'-N- ethylcarboxamidoadenosine hydrochloride (CGS-21680C), in concentrations ranging from 0.01 to 10 ${mu}M$, a recently introduced potent $A_2$ adenosine receptor agonist, increased the $[^3H]$ACh release in a dose related fashion without changing the basal rate of release. These effects were completely abolished by DMPX $(10\;{mu}M)$. In autoradiograrhy experiments, $[^3H]$2-chloro-$N^6$-cyclopentyladenosine ($[^3H]$ CCPA) bindings were highly localized in the hippocampus and the cerebral cortex. Additionally, lower levels of binding were found in the striatum. However, $[^3H]$CGS-21680C bindings were highly localized in the striatal region with the greatest density of binding found in the caudate nucleus and putamen. Lower levels of binding were also found in the nucleus accumbens and olfactory tubercle. In drug-receptor binding assay, binding of $[^3H]$ CCPA to $A_1$ adenosine receptors of rat striatal membranes was inhibited by CPA ($K_i$ = 1.6 nM) and N-ethylcarboxamidoadenosine (NECA, $K_i$ = 12.9 nM), but not by CGS-21680C ($K_i$ = 2609.2 nM) and DMPX ($K_i$ = 19,386 nM). In contrast, $[^3H]$CGS-21680C binding to $A_2$ denosine receptors was inhibited by CGS-21680C ($K_i$ = 47.6 nM) and NECA ($K_i$ = 44.9 nM), but not by CPA ($K_i$ = 2099.2 nM) and DPCPX ($K_i$ = 19,207 nM). The results presented here suggest that both types of $A_1$ and $A_2$ adenosine heteroreceptors exist and play an important role in ACh release in the rat striatal cholinergic neurons.

• The Korean Journal of Pharmacology
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• 제30권1호
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• pp.1-9
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• 1994

It has been shown that there are several subtypes of ${\kappa}$ opioid receptor. We examined ligand binding profiles and the effects of various opioid agonists on high potassium-stimulated release of $[^3H]$ histamine. We have evaluated the properties of $non-{\mu},\;non-{\delta},$ binding of $[^3H]\;DIP\;([^3H]\;diprenorphine),$ anonselective opioid antagonist, in rat cortex membranes. Binding $to\;{\mu}\;and\;{\delta}$ sites was inhibited by the use of an excess of competing selective agonists (DAMGO, DPDPE) for these sites. (-) Ethylketocyclazocine (EKC), DIP and bremazocine inhibited $[^3H]$ DIP binding. However, arylacetamides (U69593 and U50488H) gave little inhibition Replacement of sodium by NMDG and the addition of guanine nucleotide influenced the inhibitory potency of (-) EKC, an agonist for {\kappa}_1-and-{\kappa}_2-binding site, but not of bremazocine. This result suggests that bremazocine can be an antagonist at this binding site. Also, we have examined the opioid modulation of $K^+(30mM)-induced\;[^3H]\;histamine$ release in rat frontal cortex slices labeled with $1-[^3H]\;histidine$. The $[^3H]\; histamine$ release from cortex slices was inhibited by EKC in a concentration-dependent manner. However, the ${\delta}$ receptor selective agonists, DPDPE and deltorphine II, ${\mu}$ receptor agonists, DAMGO and TAPS, ${\kappa}_1-agonists$, U69593 and U50488H, and ${\varepsilon}-agonist,\;{\beta}-endorphin,$ did not. The concentration-response curve of EKC was shifted to right in the presence of naloxone, nor-binaltorphimine and bremazocine, respectively. These results suggest that ${\kappa}_2$ opioid receptor regulates histamine release in the fromtal cortex of the rat.

• Journal of Nutrition and Health
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• 제31권5호
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• pp.897-905
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• 1998

Docosahexaenoic acid(DHA), a $\omega$3 series fatty acid and arachidonic acid(AA). a $\omega$6 series fatty acid were found in relatively high concentrations in the phospholipids(PLs) of cell membranes of nerve tissues, and they can be affected by various factors. The present study examined the effects of dietary $\omega$6 and $\omega$3 fatty acid composition on P/M/S and on $\omega$3/$\omega$6 fatty acid ratios in brain PLs of 2nd generation rats. The expeimental diets consisted of 10% fat(by wt), which were computer- searched mixed oil('M') with P/M/S ratio, 1 : 1.4 : 1 and $\omega$6/$\omega$3 ratio, 6 : 1 and safflower oil('S') poor in $\omega$3 fatty acids. The experimental diets were started 3-4 wks prior to conception. During the lactation period, the feeding mothers were switched 1 wk after birth and provided the pups for 2 wks with milk which had compositions different from that of their natural mother. The same diet as their mothers was provided from weaning to 9 wks of age. The 'M'and 'S' rats were again subdivided into MM, MS, SS, SM rats according to diet which their lactating mothers were fed from the begining of the experiment. The relative percentage of P/M/S fatty acids in brain PLs in all experimental groups converged to a very similar value at 9 wks of age, indicating the existence of a control mechanism for the degree of fatty acids, unsaturation. The $\omega$3/$\omega$6 fatty acid ratios of brain PLs converged to about 1.0 in MM & SM groups and to 0.7 in SS & MS groups, suggesting also the existence of some balance between $\omega$3 and $\omega$6 fatty acids in developing rat brain. The concentrations of $\omega$3 fatty acids, especially DHA, in the SM group were increased and became similar to those in MM group at 9 wks of age. The increase in DHA of brain PLs was counterbalanced b)r a decrease in 22 5$\omega$6. Therefore, the ratios of 22 : 6$\omega$6/22 : 5$\omega$6 were higher in both MM & SM groups than those of SS & MS groups at 9 wak of age. Although dietary $\omega$3 and $\omega$6 fatty acids affected 22 : 6$\omega$S and 22 : 5$\omega$6 contained in rat brain PLs reciprocally, the relative percentage of AA did not appear to be significantly influenced by the diet in all groups at 9 wks of age, suggesting that a mechanism for the maintenance of a certain level of AA in brain PLs exists. In conclusion, the $\omega$3/$\omega$6 fatty acid and 22 : 6$\omega$3/22 : 5$\omega$6 ratios, but not P/M/S ratio, of rat brain PLs were affected by the postnatal dietary changes. Futher studies are required to clarify the mechanism(S) of ensuring a certain level of DHA and of maintaining a similar level of AA in rat brain PLs after. weaning(9 wk) regardless of prenatal and postnatal dietary changes. (Korean J Nutrition 31(5) : 897-905, 1998)

• The Korean Journal of Malacology
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• 제24권1호
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• pp.41-50
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• 2008

The histochemical characteristics and ultrastructure of the mantle in the spiny top shell, Batillus cornutus were described using light and electron microscopy. The simple epidermal layer wrapped on the top and bottom of the centrally located connective tissue. And then the epidermal layer were divided into the outer epidermal layer near a shell and the inner epidermal layer closed to the visceral mass. The connective tissue layer was composed of the collagen fiber muscularfiber bundle and hemolymph sinus. Mucous cells in the apical mantle contained acid and neutral mucopolysaccaride, and acidic carboxylated mucopolysaccaride in the mid and marginal mantle. The mantle thickness, epidermal layer thickness and hemolymph sinus area displayed a trend of reduction from the marginal zone to the apical zone. From TEM observation, it was possible to distinguish epithelium, ciliated cell, absorptive cell and secretory cell in the epidermal layer. The epithelia were columnar and the nucleus was elliptical. The free surface were covered with microvilli. The lateral membranes of epithelium was con nected with neighboring cells by the zonular occludens, zonular adherens and membrane interdigitation. Ciliated cell on free surface had cilia and microvilli, and numerous mitochondria in the apical cytoplasm. In the epidermal layer, it observed 2 type cells having absorptive function. The absorptive cells were columnar in shape, and contained microvilli, pinocytotic vesicles, mitochondria and lysosomes of various electron density. Secretory cells can be divided into four types (A, B, C, D) depending on the cell shape and characteristics of secretory granules. These cells were unicellular glands and had similar characteristics to previously reported on the mantle of the gastropod and bivalves.

• Asian-Australasian Journal of Animal Sciences
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• 제9권1호
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• pp.1-25
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• 1996

The pathogenesis of atherosclerosis can not be summarized as a single process. Lipid infiltration hypothesis and endothelial injury hypothesis have been proposed and investigated. Recent developments show that there are many points of potential interactions between them and that they can actually be regarded as two phases of a single, unifying hypothesis. Among the many risk factors of atherosclerosis, plasma homocysteine and lipoprotein(a) draw a considerable interest because they are independent indicators of atherogenicity. Triglyceride (TG)-rich lipoproteins (chylomicron and VLDL) are not considered to be atherogenic but they are related to the metabolism of HDL cholesterol and indirectly related to coronary heart disease (CHD). LDL can of itself be atherogenic but the oxidative products of this lipoprotein are more detrimental. HDL cholesterol has been considered to be a favorable cholesterol. The so-called 'causalist view' claims that HDL traps excess cholesterol from cellular membranes and transfers it to TG-rich lipoproteins that are subsequently removed by hepatic receptors. In the so-called 'noncausalist view', HDL does not interfere directly with cholesterol deposition in the arterial wall but instead reflects he metabolism of TG-rich lipoproteins and their conversion to atherogenic remnants. Approximately 70-80% of the human population shows an effective feedback control mechanism in cholesterol homeostasis. Type of dietary fat has a significant effect on the lipoprotein cholesterol metabolism and atherosclerosis. Generally, saturated fatty acids elevate and PUFA lower serum cholesterol, whereas MUFA have no specific effect. EPA and DHA inhibit the synthesis of TG, VLDL and LDL, and may have favourable effects on some of the risk factors. Phospholipids, particularly lecithin, have an antiatherosclerotic effect. Essential phospholipids (EPL) may enhance the formation of polyunsaturated cholesteryl ester (CE) which is less sclerotic and more easily dispersed via enhanced hydrolysis of CE in the arterial wall. Also, neutral fecal steroid elimination may be enhanced and cholesterol absorption reduced following EPL treatment. Antioxidants protect lipoproteins from oxidation, and cells from the injury of toxic, oxidized LDL. The rationale for lowering of serum cholesterol is the strong association between elevation of plasma or serum cholesterol and CHD. Cholesterol-lowing, especially LDL cholesterol, to the target level could be achieved using diet and combination of drug therapy. Information on the link between cholesterol and CHD has decreased egg consumption by 16-25%. Some clinical studies have indicated that dietary cholesterol and egg have a significant hypercholesterolemic effect, while others have indicated no effect. These studies differed in the use of purified cholesterol or cholesterol in eggs, in the range of baseline and challenge cholesterol levels, in the quality and quantity of concomitant dietary fat, in the study population demographics and initial serum cholesterol levels, and clinical settings. Cholesterol content of eggs varies to a certain extent depending on the age, breed and diet of hens. However, egg yolk cholesterol level is very resistant to change because of the particular mechanism involved in yolk formation. Egg yolk contains a factor of factors responsible for accelerated cholesterol metabolism and excretion compared with crystalline cholesterol. One of these factors could be egg lecithin. Egg lecithin may not be as effective as soybean lecithin in lowering serum cholesterol level due probably to the differences of fatty acid composition. However, egg lecithin may have positive effects in hypercholesterolemia by increasing serum HDL level and excretion of fecal cholesterol. The association of serum cholesterol with egg consumption has been widely studied. When the basal or control diet contained little or no cholesterol, consumption of 1 or 2 eggs daily increased the concentration of plasma cholesterol, whereas that of the normolipemic persons on a normal diet was not significantly influenced by consuming 2 to 3 eggs daily. At higher levels of egg consumption, the concentration of HDL tends to increase as well as LDL. There exist hyper-and hypo-responders to dietary (egg) cholesterol. Identifying individuals in both categories would be useful from the point of view of nutrition guidelines. Dietary modification of fatty acid composition has been pursued as a viable method of modifying fat composition of eggs and adding value to eggs. In many cases beneficial effects of PUFA enriched eggs have been demonstrated. Generally, consumption of n-3 fatty acids enriched eggs lowered the concentration of plasma TG and total cholesterol compared to the consumption of regular eggs. Due to the highly oxidative nature of PUFA, stability of this fat is essential. The implication of hepatic lipid accumulation which was observed in hens fed on fish oils should be explored. Nutritional manipulations, such as supplementation with iodine, inhibitors of cholesterol biosynthesis, garlic products, amino acids and high fibre ingredients, have met a limited success in lowering egg cholesterol.

• The Korean Journal of Pharmacology
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• 제24권1호
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• pp.53-61
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• 1988

The effect of antioxidants on the myocardial cellular damage which occurs during reoxygenation of hypoxic myocardium was examined in isolated rat hearts. The roles of oxygen free radical and lipid peroxidation in reoxygenation injury of myocardium were also investigated. In Langenorff preparation of isolated rat heart, which was made hypoxic by perfusion with the substrate free, hypoxic cardioplegic solution ($37^{\circ}C$, 90 min), the release of cytosolic enzymes (creatine phosphokinase, lactic dehydrogenase) and a lipid peroxidation product, malondialdehyde into the coronary effluent were abruptly increased by reoxygenation. The release of enzymes was closely parallel to that of MDA. These increases of enzymes and lipid peroxidation product were suppressed to various degrees in the presence of scavengers of superoxide anion (superoxide dismutase, 10,000 U), hydrogen peroxide (catalase, 25,000 U) and hydroxyl radical (dimethyl sulfoxide, 10%). A natural antioxidant, ${\alpha}-tocopherol$(4.5 uM) and a synthetic one, butylated hydroxytoluene (2 uM) suppressed the release of cytosolic enzymes with the concomittent reduction of lipid peroxidation as measured by malondialdehyde release into the coronary effluent. These effects of antioxidants were dose dependent, and were more pronounced when the antioxidants were administered throughout hypoxic and reoxygenation periods than given during reoxygenation period only. These results suggest that cytotoxic oxygen free radicals produced in the myocardium during reoxygenation may be responsible fur the myocardial cellular injury by enhancing the lipid peroxidation of cellular membranes. Furthermore, the antioxidants may exert protective effect against reoxygenation damage of hypoxic myocardium through the inhibition of lipid peroxidation reaction.

• The Korean Journal of Pharmacology
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• 제30권3호
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• pp.273-289
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• 1994

Reversible brain ischemia was produced by occluding both common carotid arteries for 5 min, and the effects of aminoguanidine (AG), $DL-{\alpha}-difluoromethylornithine$ (DFMO), MK-801, and nimodipine (NM) on the ischemia induced changes of the polyamine, glutamate and acetylcholine levels in the hippocampus CA1 subfield and the specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membranes were studied with a histological reference of the cresyl violet stained hippocampus. The basal putrescine level $(PT:\;74.4{\pm}8.8\;nM)$ showed a rapid increase (up to 1.7 fold) for 5 min of ischemia, remained significantly increased for 6 h, and then resumed the further increase to amount gradually up to about 3 fold 96 h after recirculation. However, the level of spermidine was little changed, and the spermine level showed a transient increase during ischemia followed by a sustained decrease to about 40% of the preischemic level after recirculation. The increase of PT level induced by brain ischemia was enhanced with AG or MK-801, but it was reduced by DFMO or NM. The basal glutamate level $(GT:\;0.90{\pm}0.l4\;{\mu}M)$ rapidly increased to a peak level of $8.19{\pm}1.14\;{\mu}M$ within 5 min after onset of the ischemia and then decreased to the preischemic level in about 25 min after recirculation. And NM reduced the ischemia induced increase of GT level by about 25%, but AG, DFMO and MK-801 did not affect the GT increase. The basal acetylcholine level $(ACh:\;118.0{\pm}10.5\;{\mu}M)$ did little change during/after brain ischemia and was little affected by AG or NM. But DFMO and MK-801, respectively, produced the moderate decrease of ACh level. The specific $[^3H]\;MK-801$ binding to the hippocampus synaptosomal membrane was little affected by brain ischemia for 5 min. The control value (78.9 fmole/mg protein) was moderately decreased by AG and MK-801, respectively but was little changed by DFMO or NM. The microscopic findings of the brains extirpated on day 7 after ischemia showed severe neuronal damage of the hippocampus, particularly CA1 subfield. NM and AG moderately attenuated the delayed neuronal damage, and DFMO, on the contrary, aggravated the ischemia induced damage. However, MK-801 did not protect the hippocampus from ischemic damage. These results suggest that unlike to the mode of anti-ischemic action of NM, AG might protect the hippocampus from ischemic injury as being negatively regulatory on the N-methyl-D-aspartate (NMDA) receptor function in the hippocampus.

• The Korean Journal of Physiology
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• 제18권1호
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.

• Journal of the Society of Cosmetic Scientists of Korea
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• 제38권1호
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• pp.57-65
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• 2012

In the present study, the antioxidative properties, inhibitory activity on tyrosinase, and active components of Eriobotrya japonica (E. japonica) leaf extract were investigated. The free radical (1,1-diphenyl-2-picrylhydrazyl, DPPH) scavenging activity ($FSC_{50}$) of extract/fraction of E. japonica leaf was in the order 50 % ethanol extract ($22.625{\mu}g/mL$) < ethyl acetate fraction (6.75) < deglycosylated aglycone fraction (5.06). Reactive oxygen species (ROS) scavenging activities ($OSC_{50}$) of fraction/extracton ROS generated in $Fe^{3+}-EDTA/H_2O_2$ system using the luminol-dependent chemiluminescenceassay were investigated. $OSC_{50}$ of the ethyl acetate fraction, deglycosylated aglycone fraction, and ethanol extract were 0.75, 0.79, and $1.61{\mu}g/mL$, respectively. The cellular protective effects of E. japonica leaf extract on the rose-bengal sensitized photohemolysis of human erythrocytes were investigated. The protective effects of extract/fraction of E. japonica leaf were increased in a in a concentration dependent manner ($5{\sim}50{\mu}g/mL$). Especially, ${\tau}50$ of ethyl acetate fraction at concentrations of $10{\mu}g/mL$ and $50{\mu}g/mL$ showed the most protective effects at 390.8 min and 1471.5 min. The inhibitory effect ($IC_50$) on tyrosinase of E. japonica leaf extracts was higher than arbutin, known as a skin-whitening agent. The order of inhibitory effects was acetate fraction ($75.25{\mu}g/mL$) < 50 % extract (74.1) < deglycosylated aglycone fraction (43.35). TLC of the ethyl acetate fraction showed 7 bands (EJL 1 - EJL 7). HPLC of the aglycone fraction exhibited 2 peaks, kaempferol and quercetin. The amounts of kaempferol and quercetin were 53.7 and 46.3 %. respectively. Therefore, The amounts of kaempferol and its glucoside were a little bit higher than quercetin and its glucoside in E. japonica leaf extract. Accordingly, these findings suggest that extracts/fractions of E. japonica leaf can function as antioxidants in biological systems, especially skin exposed to UV radiation, and protect cellular membranes against ROS. Thus, the extract/fraction of E. japonica leaf may be used in novel functional cosmetics as antioxidants against skin photoaging.