Aralia elata, Chaenomeles sinensis fruit, and Glycyrrhizae radix have been widely used as oriental medicinal plants in Korea, China and Japan and found to possess anti-oxidative and anti-inflammatory activities. The current study was conducted to investigate the neuroprotective effect of an ethanol extract of a mixture of A. elata, C. sinensis fruit, and Glycyrrhizae radix (ACG) against ischemia-induced brain injury in rats and excitotoxic and oxidative neuronal death in primarily cultured rat cortical neurons. Transient focal cerebral ischemia was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion (MCAO/R) in rats. Oral administration of ACG (10, 25, and 50 mg/kg) 30 min before MCAO, after 1 h of MCAO, and after 1 h of reperfusion reduced MCAO/R-induced brain infarct and edema formation. ACG also inhibited development of behavioral disabilities in MCAO/R-treated rats. Exposure of cultured cortical neurons to 500 μM glutamate for 12 h resulted in neuronal cell death. ACG (1, 10, and 50 μg/mL) inhibited glutamate-induced neuronal death. Furthermore, ACG inhibited 100 μM hydrogen peroxide (H2O2)- and hypoxia-induced neuronal death. These results suggest that the neuroprotective effect of ACG against ischemia-induced brain damage might be associated with its anti-excitotoxic and anti-oxidative activity and that ACG may have a therapeutic role for prevention of neurodegeneration in stroke.

The young shoots of Aralia elata, Chaenomeles sinensis fruit and Glycyrrhizae radix are edible and traditionally used as anti-inflammatory and antioxidant agents. The present study was performed to investigate the protective effect of an ethanol extract mixture of these three medicinal plants (ACG) against amyloid β protein (Aβ) (25– 35)-induced memory impairment in an ICR mouse model. Memory impairment was induced by intracerebroventricular microinjection of 15 nmol Aβ (25–35) and assessed using the passive avoidance test and the Morris water maze test. The step-through latency in the passive avoidance test was decreased and the latency to reach the hidden platform in the Morris water maze test was increased in mice treated with Aβ (25–35), indicating memory impairment. This memory impairment induced by Aβ (25–35) was significantly prevented by chronic treatment with ACG (10, 25, and 50 mg/kg, p.o., 8 days). In memory impaired mice brain, cholinesterase activity and concentration of thiobarbituric acid reactive substance, a lipid peroxidation marker, were increased and glutathione level was decreased. These biochemical changes in Aβ (25–35)-treated mice were reversed by chronic administration of ACG. The present results suggest that antioxidant and anti-cholinesterase activities of ACG might be responsible for the inhibition of Aβ (25– 35)-induced memory impairment and that ACG preparation may have a therapeutic role in preventing the progression of Alzheimer’s disease.

Actinidia arguta (Actinidiaceae), which is commonly referred to as hardy kiwifruit, has been reported to possess anti-inflammatory, anti-allergic and antioxidative properties. The protective effect of the leaves and stems of A. arguta against amyloid β protein (Aβ) (25-35)-induced cultured neuronal cell death and memory impairment was investigated in the current study. Exposure of cultured cortical neurons to 10 μM Aβ (25-35) for 24 h induced significant neuronal death as assessed by a 3-[4,5-dimethylthiazol- 2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. However, A. arguta (10 and 50 μg/ ml) prevented Aβ (25-35)-induced apoptotic neuronal death in cultured cortical neurons. A. arguta also inhibited the 100 μM H2O2-induced decrease of the MTT reduction rate in cultured neurons. Memory impairment was produced by intracerebroventricular microinjection of 15 nmol Aβ (25- 35) and examined using the passive avoidance test in ICR mice. Chronic treatments with A. arguta (50 and 100 mg/ kg, 14 days, p.o.) significantly prevented memory impairment induced by Aβ (25-35), and A. arguta inhibited the Aβ (25-35)-induced increase of cholinesterase activity in the brains of memory impaired mice. These results suggest that A. arguta might be able to inhibit Aβ (25-35)-induced neuronal death and memory impairment via antioxidative and anti-cholinesterase effects and that A. arguta could have a therapeutic role for preventing the progression of neurodegeneration in Alzheimer’s disease.

Vitis amurensis, Aralia cordata, and Glycyrrhizae radix have been widely used in Korea, China, and Japan because of their anti-oxidative and anti-inflammatory activities. The present study investigated the anti-nociceptive and antiinflammatory properties of an ethanol extract (SSB) of a mixture of three medicinal plants of Vitis amurensis (stem and leaf), Aralia cordata (stem and leaf), and Glycyrrhizae radix. Anti-nociceptive activity was determined using chemical (acetic acid and formalin) and thermal (hot plate) stimuli-induced algesia tests. Formalin-induced paw edema was evaluated for anti-inflammatory activity. SSB (25–100 mg/kg, p.o.) and ibuprofen (100 mg/kg, p.o.), a positive nonsteroidal anti-inflammatory drug (NSAID), significantly inhibited the acetic acid-induced writhing response caused by peripherally mediated algesia, but failed to protect thermal nociception in the hot plate test that was employed for centrally mediated analgesic activity. However, morphine (5 mg/kg, s.c.) used as a positive opioid control alleviated the acetic acid-induced writhing response and thermal nociception in the hot plate test. In the formalin test, SSB (50 and 100 mg/kg, p.o.) inhibited the second phase response (peripheral inflammatory algesia), but not the first phase response (central algesia), whereas morphine inhibited both phases of the pain response. Both SSB (25-100 mg/kg, p.o.) and ibuprofen (200 mg/kg) caused significant reduction of the formalin-induced increase of paw thickness, which was the index of inflammation. These results suggest that SSB has a significant anti-nociceptive activity that seems to be peripheral, but not central. SSB also displays antiinflammatory activity in an acute inflammatory model. The present study supports a possible use of SSB to treat pain and inflammation.

Alzheimer’s disease (AD), a progressive neurodegenerative disorder that deprives the patient of memory, is associated mainly with extracellular senile plaque induced by the accumulation of amyloid β protein (Aβ). Silybum marianum (Asteraceae; SM) is a medicinal plant that has long been used in traditional medicine as a hepatoprotective remedy owing to its antioxidant and anti-inflammatory activities. The present study examined the methanol extract of the aerial parts of SM for neuroprotection against Aβ (25-35)-induced neuronal death in cultured rat cortical neurons to investigate a possible therapeutic role of SM in AD. The primary cortical neuron cultures were prepared using embryonic day 15 to 16 SD rat fetuses. Cultured cortical neurons exposed to 10 μM Aβ (25-35) for 36 h underwent neuronal cell death. At 10 and 50 μg/mL, SM prevented Aβ (25-35)-induced neuronal cell death and apoptosis in cultured cortical neurons. Furthermore, SM inhibited the Aβ (25-35)-induced decrease in anti-apoptotic protein, Bcl-2, and the increase in the proapoptotic proteins, Bax and active caspase-3. Cultured cortical neurons exposed to 1 mM N-methyl-D-aspartate (NMDA) for 14 h induced neuronal cell death. SM (10 and 50 μg/mL) prevented NMDA-induced neuronal cell death. These results suggest that SM inhibited Aβ (25-35)-induced neuronal apoptotic death via inhibition of NMDA receptor activation and that SM has a possible therapeutic role in preventing the progression of neurodegeneration in AD.

Vitis amurensis, Aralia cordata, and Glycyrrhizae radix have been widely used as oriental medicinal plants in Korea, China and Japan and found to possess anti-oxidative and anti-inflammatory activities. A previous study demonstrated a protection of an ethanol extract (SSB) of a mixture of three medicinal plants of Vitis amurensis, Aralia cordata, and Glycyrrhizae radix against β amyloid protein-induced memory impairment. The current study was conducted to investigate the neuroprotective effect of SSB against ischemiainduced brain injury. Transient focal cerebral ischemia was induced by 2 hr middle cerebral artery occlusion followed by 24 hr reperfusion (MCAO/reperfusion) in rats. Oral administration of SSB (5, 10 and 25 mg/kg) 30 min before and 1 h after MCAO, and 1 h after reperfusion reduced MCAO/ reperfusion-induced brain infarct and edema formation. SSB also inhibited development of behavioral disabilities in MCAO/reperfusion-treated rats. Exposure of cultured cortical neurons to 500 μM glutamate for 12 hr resulted in neuronal cell death. SSB (1-10 μg/mL) inhibited glutamateinduced neuronal death, elevation of intracellular calcium concentration ([Ca2+]i), and generation of reactive oxygen species (ROS). These results suggest that the neuroprotective effect of SSB against ischemia-induced brain damage might be associated with its anti-excitotoxic activity and that SSB may have a therapeutic role for prevention of neurodegeneration in stroke.

The study investigated the effects of trans-ε-viniferin on in vitro maturation (IVM) and gene expression. Three experiments were conducted. Firstly the trans-ε-viniferin was purified from the leaves and stems of the Vitis amurensis , a common wild grape found in Korea, Japan, and China. In the first experiment, a total of 594 cumulus oocytes complexes (COCs) were used for the evaluation of the nuclear maturation. COCs were matured with various concentrations of trans-ε-viniferin (0, 0.1, 0.5, 1.0 and 5.0 μM). After IVM 42 44 h, the nuclear maturation was evaluated. In the second experiment, a total of 300 matured oocytes were used to examine the effects of different trans-ε-viniferin concentrations (0, 0.5 and 5.0 μM) on porcine oocyte intracellular GSH and ROS levels. In the third experiment, the gene expression of oocytes matured with trans-ε-viniferin (0.5 μM) and the untreated group were evaluated after IVM. As results, we observed that trans-ε- viniferin treatment during IVM did not improve the nuclear maturation. But significantly increased (p<0.05) intracellular GSH levels in 0.5 μM group (0 μM vs. 0.5 μM; 14.6 vs. 16.8 pmol/oocyte) and reduced ROS levels (0 μM vs. 0.5 μM and 50 μM; 174.6 vs. 25.7 and 23.8 pixel/oocyte). The trans-ε-viniferin treatment during IVM of recipient oocytes promoted higher (p<0.05) expression of Dnmt1 mRNA in 0.5 μM treatment group than in the control group. But, the other gene expressions (PCNA, OCT4, caspase3, BAK, BAX and sit1) did not significantly differ from the control. In conclusion, these results indicated that the trans-ε-viniferin treatment during porcine IVM increased the cytoplasmic maturation through increasing the intracellular GSH synthesis, reducing ROS levels and increasing the Dnmt1 gene expression.

Background : Alzheimer`s disease (AD) is characterized by neuronal loss and extracellular senile plaque, whose major constituent is β-amyloid (Aβ), a 39-43 amino acid peptide derived from amyloid precursor protein. In cultures, Aβ directly induce neuronal cell death and can include excessive generation of free radicals and peroxidative injury to proteins, lipids, and other macromolecules. Actinidia arguta, generally called hardy kiwifruit, has been reported to possess anti-inflammatory, anti-allergic and antioxidative properties. The present study aims to investigate the neuroprotective effect of the leaves and stems of A. arguta using in vitro cultured neurons and in vivo experimental animals. Methods and Results : Primary cortical neuronal cultures were prepared using Sprague-Dawley (SD) rat fetuses on embryonic days 15. Neurotoxicity experiments were performed on neurons after 3-4 days in culture. Cultured neurons were treated with 10 μM Aβ (25-35) for 24 h to produce neurotoxicity. In addition, cultured neurons were treated with H2O2 (100 μM) for 15 min and then incubated for 12 h in H2O2-free medium. Viability of cultured neurons was measured by a colorimetric MTT assay. Hoechst 33342 staining of neurons was carried out to examine Aβ (25-35)-induced apoptotic neuronal death. A. arguta over the concentration of 10 to 50 ㎍/㎖ prevented Aβ (25-35) (10 μM)-induced apoptotic neuronal death, and inhibited H2O2-induced decrease of MTT reduction rate. These results suggest that oxidative stress is implicated in Aβ (25-35)-induced neuronal apoptotic death. Memory impairment was produced by intracerebroventricular (i.c.v) microinjection of 15 nmol Aß (25-35) and examined using passive avoidance test in ICR mice. Chronic treatments with A. arguta (14 days, p.o.) protected memory impairment induced by Aß (25-35). Conclusion : The present study suggests that A. arguta has a therapeutic role for preventing the progression of neurodegenerative disease such as AD.

Background : It is well known that Alzheimer`s disease (AD) is associated with neuronal loss and accumulation of extracellular senile plaque, whose major constituent is β-amyloid peptide (Aβ). In cell cultures, Aβ can directly stimulate neuronal cell death and make neurons susceptible to excitotoxicity which may include glutamate release and N-methyl-D-aspartate (NMDA) receptor activation. There are numerous reports in the literature of Cedrela sinensis (CS) for pro-apoptotic effects. It was hypothesized that CS might protect neurons against neurodegeneration in AD due to its pro-apoptotic effects. The current study aimed to determine the protective effect of ethanol extract from the leave of CS on Aβ (25-35)-induced neuronal cell death in primary cultured rat cortical neurons. Methods and Results : Cerebral neurons were collected from embryonic day 15 SD rat fetuses and were cultured on DMEM with serum. Neurotoxicity experiments were proceeded on cultured neurons after 4-5 days in vitro. Cultured neurons were treated with 10 μM Aβ (25-35) for 24 h or 1 mM NMDA for 20 h to induce neuronal death. CS was applied 20 min before the treatment with Aβ (25-35) or NMDA and also present in the medium during the incubations. Colorimetric MTT assay and Hoechst 33342 staining were used to estimate viability of neurons. Western blot analysis was carried out to examine the expression levels of anti-apoptotic and pro-apoptotic proteins. CS (5 and 10 ㎍/㎖) significantly inhibited Aβ (25-35)-induced apoptotic neuronal cell death in cultured cortical neurons. CS also inhibited Aβ (25-35)-induced change of apoptosis-related protein expression in western blot analysis. Furthermore CS (5 and 10 ㎍/㎖) reuduced NMDA-induced neuronal cell death. This study demonstrated that NMDA glutamate receptor activation is related with Aβ (25-35)-induced neuronal apoptotic death. Conclusion : CS protected culterd neurons against Aβ (25-35)-induced neurotoxicity probably via inhibition of NMDA receptor activation. These results suggest that CS can prevent the progression of neurodegenerative disease such as Alzheimer's disease.

Background : Alzheimer`s disease (AD) is characterized by neuronal loss and extracellular senile plaque, whose major constituent is β-amyloid (Aβ), a 39-43 amino acid peptide derived from amyloid precursor protein. In cultures, Aβ can directly induce neuronal cell death and can render neurons vulnerable to excitotoxicity which may involve glutamate release and N-methyl-D-aspartate (NMDA) receptor. Silybum marianum (SM) has been used for centuries to treat liver disease due to its antioxidant, and anti-inflammatory properties. In particular, Silymarin, an active constituent of SM, has been reported to decrease lipid peroxidation. Therefore we hypothesized that SM might protect neurons against neurodegeneration in AD due to its antioxidant and anti-inflammatory activities. In the present study, the protective effect of ethanol extract from the stem of SM on Aβ (25-35)-induced neuronal cell death was examined in primary cultured rat cortical neurons. Methods and Results : Primary cultured cortical neurons were prepared using embryonic day 15 SD rat fetuses. Neurotoxicity experiments were performed on cultured neurons after 4-5 days in vitro. The cells were treated with 10 μM Aβ (25-35) or 1 mM NMDA for 36 h or 14 h, respectively. SM was applied 15 min before treatment of Aβ (25-35) or NMDA and also present in the medium during the incubations. The viability of neurons was monitored using a colorimetric MTT assay and Hoechst 33342 staining. The expression levels of anti-apoptotic and pro-apoptotic proteins were detected by western blot. An Ethanol extract of the stem of SM (10 and 50 μg/ml) significantly prevented Aβ (25-35)-induced apoptotic neuronal cell death in cultured cortical neurons. Furthermore SM inhibited Aβ (25-35)-induced decrease of anti-apoptotic protein, Bcl-2, and increase of pro-apoptotic proteins, Bax and active caspase-2, in western blot analysis. SM (10 and 50 μg/ml) also reduced NMDA-induced neuronal cell death. These results suggest that NMDA glutamate receptor activation is implicated in Aβ (25-35) -induced neuronal apoptotic death. Conclusion : The present study suggests that SM has a possible therapeutic role for preventing the progression of neurodegenerative disease such as Alzheimer's disease.

Background : Ischemic stroke is a common cause of adult disability and death worldwide. Excessive oxidative stress is an important pathogenic mechanism in ischemic stroke. Major reduction of endogenous antioxidative systems increases production of free radicals inducing peroxidation of lipid, protein, and nucleic acid. 1,3-Dipalmitoyl-2-oleoylglycerol (DPOG) is a triglyceride found in oils from various natural sources such as palm kernels, sunflower seeds and rice bran. We found DPOG as an active constituent of rice bran oil. In the present study, we investigated neuroprotective effect of DPOG derived from rice bran oil on excitotoxicity in cultured neurons and on ischemic brain injury in rats. Methods and Results : Transient focal ischemic brain damage was induced by 2 h middle cerebral artery occlusion followed by 24h reperfusion (MCAO/reperfusion) in rats. After MCAO/reperfusion, the infarct and edema volume of brain tissue was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining methods. Glutathione concentration and lipid peroxidation rate were measured in brain tissue. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in brain tissue were detected by Western blot. Cerebral cortical neuronal cells were cultured in 15-days-old fetus. Cortical neurons were incubated with 1 mM N-methyl-D-aspartate (NMDA) for 14 h to produce excitotoxicity. Cell viability was measured by MTT assay. DPOG (1-5 mg/kg) significantly reduced MCAO/reperfusion-induced infarction and edema formation, neurological deficits, and brain cell death. Depletion of glutathione level and lipid peroxidation induced by MCAO/reperfusion were inhibited by administration of DPOG. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in ischemic brain were significantly inhibited by treatment with DPOG. DPOG (0.1-10 uM) inhibited 1 mM NMDA-induced neuronal cell death in cultured cortical neurons. Conclusion : From the above results, the present study provides an evidence that DPOG derived from rice bran oil might be effectively applied for the treatment of ischemic stroke.

Background : Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive memory loss, cognitive impairment and personality defects accompanied by diffuse structural abnormalities in the brain. The major pathological hallmarks of AD include beta amyloid (Aß) protein deposition, presence of neurofibrillary tangles and neurodegeneration of cholinergic neurons. Aß, a 39-43 amino acid proteolytic fragment of amyloid precursor protein, is the major constituent of the senile plaques. Rice bran, the major byproduct of the rice milling industry, is the source of a high quality vegetable oil. Rice bran oil (RBO) has attracted much medicinal attention for its strong hypocholesterolemic properties because of its balanced fatty acid composition and high levels of antioxidant phytochemicals such as oryzanols, tocopherols and tocotrienols. The present study aims to investigate the protective effect of RBO against Aß (25-35)-induced neurotoxicity in in vitro and in vivo. Methods and Results : Memory impairment was produced by intracerebroventricular (i.c.v) microinjection of 15 nmol Aß (25-35) and measured by passive avoidance test in ICR mice. Glutathione concentration, lipid peroxidation rate and acetylcholine esterase activity were measured in mice brain. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in mice brains were detected by Western blot. Cerebral cortical neuronal cells were cultured from 15-days-old fetus. Cortical neurons were incubated with 10 μM Aß (25-35) for 36 h. Cell viability was measured by MTT assay. Chronic treatments of RBO (0.1-1 ml/kg, 8 days, p.o.) protected against memory impairment induced by Aß (25-35). Depletion of glutathione level, lipid peroxidation and increased acetylcholine esterase activity by the treatment with Aß (25-35) were inhibited by administration of RBO. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in Aß (25-35)-administered mice brain were significantly inhibited by treatment with RBO. RBO (0.1-5ul/ml) inhibited 10μM Aß (25-35)-induced neuronal cell death in cultured cortical neurons. Conclusion : The present study suggests the role of RBO as a promising therapeutic for neurodegenerative diseases like AD and stroke.

Background : Rice bran is the outer brown layer of the rice grain and produced when rice is milled. The basic components of rice bran are fiber, lipids, amino acids, vitamins, and minerals. The oil extracted from this bran is called rice bran oil. Although whole rice bran in itself does not have anti-cholesterol properties, its oil offers significant benefits. Ischemic stroke is a major cause of morbidity and mortality worldwide. The cessation or critical reduction of blood flow in brain during acute stroke results in deprivation of the oxygen and glucose supplies, which can produce a local brain ischemia and injury. It is well established that excitotoxicity, a type of neurotoxicity evoked by elevated extracellular glutamate level, is a primary contributor to ischemic neuronal death. The present study aims to investigate the neuroprotective effect of Rice bran oil (RBO) on ischemic brain injury in rats and on excitotoxicity in cultured neurons. Methods and Results : Transient focal ischemic brain damage was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion (MCAO/reperfusion) in rats. After MCAO/reperfusion, the infarct and edema volumes of brain tissues were measured using 2,3,5-triphenyltetrazolium chloride (TTC) staining methods. The expression levels of phosphorylated mitogen activated proteins kinases (MAPKs), inflammatory factors, and anti-apoptotic and pro-apoptotic proteins in brain tissue were detected by Western blot. Primary cortical neuronal cultures were prepared using SD rat fetuses on embryonic days 15. Cortical neurons were treated with N-methyl-D-aspartate (NMDA) (1 mM) for 14 h to produce neuronal cell death. Cell viability was measured by MTT assay. RBO inhibited the formation of infartion and edema in MCAO/reperfusion–induced ischemic brains. The increase of phosphorylated MAPKs, inflammatory factors, and proapoptotic proteins and the decrease of antiapoptotic protein in ischemic brains were significantly inhibited by treatment with RBO. RBO (0.01-1ul/ml) inhibited 1 mM NMDA-induced neuronal cell death in cultured cortical neurons. Conclusion : These results suggest that RBO might be a promising therapeutic for neurodegenerative disease such as stroke.

Background : Clematis trichotoma is a deciduous climber belonging to the family Ranunculaceae. This study was carried out to survey the effect of shading levels on growth characteristics in Clematis trichotoma seedling. Methods and Results : Seeds were collected from plants growing in the Mt. Kariwang Jeongseon, Gangwon-do in October 2013, and they were sown to 96 cell plug tray filled with Peatmoss (TKS-2) soil at March, 2015. The experiment was performed with four different shading levels (0, 30, 60, 90%) at July, 2015. According to the experiment, plant height was the highest under 90% of shading. It was found that fresh weight and dry weight of clematis trichotoma were the highest under 90% of shading. The leaf number was the highest under 30% of shading. The leaf number decreased as the shading level increased. Root number and length were the highest under 90% of shading. Conclusion : According to the results, Clematis trichotoma seedling showed the highest growth under 90% shading.

Background : Scrophularia koraiensis is a herbaceous perennials belonging to the family Scrophulariaceae. This study was carried out to survey the effect of soil types on growth characteristics in Scrophularia koraiensis seedling. Methods and Results : Seeds were collected from plants growing in the Mt. Kariwang Jeongseon, Gangwon-do in September 2014, and they were sown to 128 cell plug tray filled with Peatmoss (TKS-2) soil at March, 2015. The experiment was performed with four different soil types (Peatmoss, Peatmoss + Perlite, Peatmoss + Granite soil, Commercial soil). According to the experiment, stem diameter was the highest under commercial soil. The leaf width and length were the highest under commercial soil. Main root diameter and lengh were the highest under commercial soil. Conclusion : According to the results, Scrophularia koraiensis seedling showed the highest growth in commercial soil.

Background : Scrophularia koraiensis is a herbaceous perennials belonging to the family Scrophulariaceae. This study was carried out to survey the effect of LED on root develop characteristics in Scrophularia koraiensis seedling. Methods and Results : Seeds were collected from plants growing in the Mt. Kariwang Jeongseon, Gangwon-do in September 2014, and they were sown to 128 cell plug tray filled with Peatmoss (TKS-2) soil at March, 2015. The experiment was performed with three different LED (Blue, Red, Blue + Red) at July, 2015. Morphological characteristics of root (total root length, root projet area, root surface area, root diameter and root volume) were analyzed with WinRHIZO software. Seedling root growth of scrophularia koraiensis was surveyed to be the highest at the Blue + Red LED in all measuring. Total root length was measured high in the order of Blue + Red, Red, Blue LED. Conclusion : According to the results, Scrophularia koraiensis seedling showed the highest root growth in Blue + Red LED.