Cognitive impairment is considered to be key research topics in the field of neurodegenerative diseases and in understanding of learning and memory. In the present study, we investigated neuroprotective effects of Schisandra chinensis (SC) and Ribes fasciculatum (RF) extracts in hydrogen peroxide-induced neuronal cell death in vitro and scopolamine-induced cognitive impairment in Sprague Dawley® (SD) rat in vivo. Apoptotic cell death in neuroblastic PC12 cell line was induced by hydrogen peroxide for 1 hour at 100 μM. However, mixture of SC and RF treatment prevented peroxide induced PC12 cell death with no neurotoxic effects. For in vivo experiment, the effect of SC and RF extracts on scopolamine-induced cognitive impairment in SD rat was evaluated by spontaneous alternation behavior in Y-Maze test. After 30 min scopolamine injection, the scopolamine-induced rats presented significantly decreased % spontaneous alteration and acetylcholine level, compared to non-induced group. However, treatment of SC+RF extracts rescued the reduced % spontaneous alteration with acetylcholine concentration from hippocampus in scopolamineinduced rats. These results suggested that mixture of SC and RF extract may be a potential natural therapeutic agent for the prevention of cognitive impairment.

This study was conducted to evaluate the functionality of fermented black garlic extracts under various conditions. Black garlic powder was prepared by aging for 0~72 hours at 80℃ depending on relative humidity (RH). It showed the highest antioxidant effects among the samples; the total antioxidant activity of black garlic powders at RH 75%, 84%, and 90% for 72 hours was increased 31.9 times, 28.2 times, and 22.6 times compared with that of the fresh garlic powder, respectively. Also, the alliin content was gradually decreased. S-ally-L-cysteine and S-ethyl-cysteine levels were increased; the highest values were 495.9 μg/g and 1,769.7 μg/g after aging for 72 hours at RH 75%. Aspartate transaminase (AST) and alanine transaminase (ALT) levels were increased following high fat diet feeding, but the rise was obviously reduced by administration of black garlic extract. The total cholesterol, LDL/VLDL-cholesterol, and triglyceride contents in serum were significantly lower in methionine and choline deficient (MCD) diet treatment groups than in the positive control group. The concentration was increased following the intake of black garlic and fermented black garlic extracts. Therefore, black garlic extracts could be an ideal material as a dietary supplement in healthy functional foods to improve the effects on fatty liver.

국내에서 오래 전부터 오미자와 칠해목은 약용식물로 이용해져 왔다. 오미자의 경우 생리활성 물질인 lignan을 통하여 여러가지 효능들이 연구를 통하여 알려졌으나, 칠해목의 경우 항염증과 관련된 연구가 진행되었을 뿐, 산화 스트레스와 관련된 연구는 미비한 실정이었다. 이에 본 연구에서는 오미자․칠해목의 추출혼합물을 이용하여, 과산화수소로 산화 스트레스가 유도된 SH-SY5Y 신경세포에서의 보호 효과를 알아보고자 하였다. 과산화수소의 처리 농도의 경우, 신경세포 독성 실험을 통하여 100 μM의 농도를 본 연구에 사용하였다. 또한, 오미자와 칠해목 추출물은 SH-SY5Y 신경세포에서 세포 독성이 없음을 실험을 통해 확인하였으며, 과산화수소를 이용한 신경세포 보호효과를 확인한 결과, 30% 에탄올 추출물 50 μg/mL의 농도에서 각각의 추출물에서 가장 높은 보호 효과를 확인할 수 있었다. 이에 오미자․칠해목 추출혼합물의 최적 효능 비율을 알아보기 위해서 각각의 추출물을 다양한 수율로써 6:4, 7:3, 8:2의 비율로 신경세포 보호 활성을 확인한 결과, 오미자와 칠해목 7:3의 비율과 50 μg/mL의 농도에서 가장 높은 신경세포 보호효과가 나왔으며, 이에 본 연구에서 오미자․칠해목 추출혼합물의 최적의 비율과 처리 농도로 사용하였다. Annexin V와 PI를 이용한 SH-SY5Y 신경 세포의 세포사멸을 확인해 본 결과에서도 오지마․칠해목 추출혼합물은 SH-SY5Y 신경세포의 세포사멸를 억제시키는 것을 확인할 수 있었다. 이에 본 연구에서는 오미자․칠해목 추출혼합물이 과산화수소로 유도된 산화적 스트레스에서 SH- SY5Y 신경세포에서 보호 효과가 있다는 것을 확인할 수 있었지만, 그에 대한 메카니즘에 대한 연구는 미비한 실정이다. 이에 차후 연구에서는 오미자․칠해목 추출혼합물의 산화 스트레스에 대한 정확한 기전을 파악하기 위하여 In vitro와 In-vivo에서의 후속적 연구가 필요하다고 사료된다.

알츠하이머병의 발병원인과 기전에 대하여 많은 연구가 진행되었으나, 아직까지 완전히 밝혀지지 않고 있다. 이에 본 연구에서는 STZ로 유도된 세포독성으로부터 노인성 질병의 예방과 항산화 효과로 잘 알려진 비타민 C를 이용하여 SH-SY5Y 신경세포 내 보호 기전을 살펴보고자 하였다. 본 연구 결과에 의하면, STZ를 SH-SY5Y 신경세포에 처리하였을 때, 세포사멸이 유도되는 것을 확인하였으며, 비타민C를 전처리함으로써 세포생존도가 증가하는 것을 확인하였다. 비타민 C가 신경세포를 보호하는 기전을 알아보기 위하여 세포자멸사 과정에서 신호전달을 통해 다양한 유전자를 발현시키는 MAPKs의 인산화를 살펴보았다. 비타민 C 처리시 ERK의 인산화가 증가하며, 세포증식을 유도하는 것으로 확인하였으며, ERK와는 반대로 염증, 세포사멸과 관련된 JNK의 인산화는 비타민 C에 의해 인산화가 억제되는 것으로 확인되었다. 또한 STZ는 Bax 단백질의 발현 증가와 Bcl-2 단백질의 발현을 감소시켰으며, apoptosis antibody array로 확인한 결과, Cytochrome C가 유도됨을 확인하였다. 이뿐만 아니라, 비타민 C 처리에 의해 Bcl-2가 증가하여 세포사멸이 억제되는 것을 확인하였으며, 항산화 효소인 Sod-1의 발현을 증가하는 것 또한 확인하였다. 이는 비타민 C가 항산화 방어체계를 강화시켜 STZ에 의한 세포손상을 보호하는 것으로 사료된다. 본 연구를 통하여 STZ로 유도된 SH-SY5Y 신경세포 손상 에서 비타민 C가 여러 기전을 통하여 세포자멸사를 억제하여 세포를 보호하는 효과가 있는 것을 확인할 수 있었다. 그러나 연구는 일부 기전들만을 확인한 것으로 추후 연구에서는 다양한 비타민 C의 농도 및 처리시간에 따른 기전의 차이를 분석하고, 실험동물을 통한 검증 및 스트렙토조토신에 의한 아밀로이드베타와 타우의 관련성을 확인하고자 한다.

Amyloid-β protein (Aβ) is known to increase free radical production in neuronal cells, leading to cell death by oxidative stress. The purpose of this study was to evaluate the protective effects of PineXol® on Aβ25-35 induced neuronal cell death. Rat pheochromocytoma (PC-12) cells were pre-treated with 100 μg/mL of PineXol® for 2 h. The cells were exposed to single dose of 30 μM Aβ25-35 for 24 h. Cell death was assessed by a cell count kit-8 (CCK-8) assay, lactate and dehydrogenase (LDH) release assay. An Apoptotic process was analyzed by a protein expression of the Bcl-2 family using western blotting. Cell viability increased in PC-12 cells treated with both Aβ25-35 and PineXol®, compared to the control group. PineXol® induced a decrease of the Bcl-2 protein expression (p<0.05), while Bax and Sod1 increased (p<0.05), indicating attenuation of Aβ25-35 induced apoptosis. These results suggest that PineXol® may be a good candidate for the prevention of Alzheimer’s disease(AD).

The purpose of this study was to evaluate the protective effect of PineXol® on H2O2-induced cell death in SK-N-MC cells, and in early stage focal ischemia rodent model. SK-N-MC cells were pre-treated with 200 μM H2O2 or various concentrations of PineXol® (10, 30, and 50 pg/mL) for 24 h, and then exposed to H2O2 for 3 h. Cell death was assessed by the CCK-8 assay, reactive oxygen species (ROS) assay, and lactate and dehydrogenase (LDH) release assay. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) expressions were also analyzed by western blotting. Focal ischemia rodent model was used as the in vivo model, and different concentrations of PineXol® (1, 10, and 100 mg/kg) were administered. One week after administration, reduction of infarct volume was analyzed by TTC staining. Cell viability of H2O2-treated SK-N-MC cells significantly increased by pre-treatment of PineXol® (p<0.05). PineXol® pre-treatment also induced significant decrease of ROS and LDH expressions. However, PineXol® did not affect the infarct volume. These results suggest that PineXol® has significant neuroprotective effect in vitro, but statistical significance was not confirmed in the in vivo focal ischemia mo

Menopausal status and hormonal changes are important factors related to the prevalence of metabolic syndrome in women. Nutrient intake is also a risk factor for metabolic syndrome. Although, postmenopausal status and hormonal changes result in a 60% increased risk for metabolic syndrome, there has been no method to elucidate the effects of nutrient intake on metabolic syndrome following menopause. This study was conducted to evaluate the effects of nutrient intake by menopausal women on the prevalence of metabolic syndrome. All data were obtained from the Korean National Health and Nutrition Examination Survey 2007–2009. Menopausal women showed a 1.8-fold increase in the prevalence of metabolic syndrome. Metabolic syndrome group showed significantly lower values in calcium, iron, vitamin A, carotin, retinol and riboflavin intake than those of normal group in premenopausal women. In postmenopausal women, there are significant differences in crude fiber, calcium, iron, potassium, riboflavin and niacin. Indeed, different patterns of nutrient intake were observed by menopausal status and metabolic syndrome. As menopause cannot be controlled, a diet with adequate nutrient intake may be useful to control the rapid increase in the prevalence of metabolic syndrome due to menopause.

This study was conducted to evaluate the neuroprotective effects of Cheonggukjang extract in in-vitro and in-vivo models. T98G-human glioblastoma cells were pretreated with various concentrations (1~10 mg/mL) of Cheonggukjang extract for 24 h and then exposed to H2O2 (1 mM) for 3 h. The neuroprotective effects of Cheonggukjang extract were measured using a CCK-8 kit assay, total antioxidant capacity (TAC) assay, reactive oxygen species (ROS) assay, and lactate dehydrogenase (LDH) release assay. The early stage focal ischemia rodent model was used as the in-vivo neurotoxicity model. Various concentrations (10~200 mg) of Cheonggukjang extract were administered to the animal models for 1 week. Peripheral blood was analyzed for glutathione peroxidase (GPx) expression by ELISA, and infarct volume reduction was analyzed by TTC staining. Cheonggukjang extract significantly (p<0.05) increased cell viability in T98G cells against H2O2 as well as against the induced neurotoxicity. Indeed, treatment with the Cheonggukjang extract induced a decrease in ROS and LDH expression and increased TAC significantly (p<0.05). However, Cheonggukjang extract did not induce a decrease in infarct volume or an increase in GPx expression in the in-vivo model. Despite the limitation in neuroprotection, Cheonggukjang extract may be useful for treating ROS injury.