Background: Cisplatin is one of the most extensively used chemotherapeutic agents for the treatment of cancer, including bladder, and ovarian cancers. However, it has been shown to induce nephrotoxicity, despite being an outstanding anti-cancer drug. In this study, we investigated the protective effect of dopaol β-D-glucoside (dopaol) on cisplatin-induced nephrotoxicity. Methods and Results: To confirm the protective effect of dopaol on cisplatin-induced nephrotoxicity, HK-2 cells were treated with 20 μM cisplatin and 80 μM dopaol. Cisplatin increased apoptosis, caspase-3 activity and mitochondrial dysfunction; however pretreatment with 80 μM dopaol successfully attenuated apoptosis, caspase-3 activity and mitochondrial dysfunction. To evaluate the protective effect dopaol on cisplatin-induced nephrotoxicity in vivo, we used an animal model (balb/c mice, 20 ㎎/㎏, i.p. once/day for 3 day). The results were similar to those obtained using HK-2 cells; renal tubular damage and neutrophilia induced by cisplatin reduced following dopaol injection (10 ㎎/㎏, i.p. once/day for 3 day). Conclusions: These results indicate that dopaol treatment reduced cisplatin-induced nephrotoxicity in vitro and in vivo, and can be used to treat cisplatin-induced nephrotoxicity. However, further studies are required to determine the toxicity high dose dopaol and the signal pathways involved in its mechanism of action in animal models.

This study aimed to investigate the various biological activities of Geranium thunbergii such as antimicrobial activity and protective effect against oxidative damage. To evaluate its antioxidant and antimicrobial activities, we first performed methanol extraction; this methanol extract was further partitioned using various solvents. And then, its antioxidant activity was measured using various assays including total phenolic content and protection against oxidative DNA damage, and antimicrobial activities were examined using minimum inhibiting concentration (MIC) test, and paper disc method. In addition, high-performance liquid chromatography was performed to analyze the major chemical components of ethyl acetate fraction. The G. thunbergii fraction with ethyl acetate exhibited higher antioxidant and antimicrobial activities than the other fractions. The results showed that G. thunbergii ethyl acetate fraction at 50 μg/mL had strong DPPH and ABTS radical scavenging activities of 80.88% and 80.12%, respectively. In addition, the ethyl acetate fraction protected DNA from the oxidative damage induced by ferrous ion and hydroxyl radicals and showed high antimicrobial activity with diameter of inhibition zones ranging from 13.33 to 15.67 mm. High-performance liquid chromatography analysis revealed the major phenolic compounds of G. thunbergii to be ellagic acid and gallic acid. These results suggest that G. thunbergii might protect DNA against oxidative stress induced by reactive oxygen species and can be utilized as a natural source of antioxidant and antimicrobial agent in the food industry.

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.

동물실험에서 실크단백질 산 가수분해물을 투여하고 t-BHP투여한 군의 혈액 생화학적 검사 결과t-BHP만 투여한 군과 비교하였을 때 AST, ALT 그리고 LDH가 실크단백질 산 가수분해물의 투여 농도가 높아질수록 수치가 감소하는 것으로 나타났고 세포가 손상할 시에 증가하는 MDA를 간 조직을 대상으로 측정한 결과 실크단백질 산 가수분해물의 농도가 높아질수록 수치가 대조군과 유사한 정도로 감소하는 것으로 보아 간 손상에 관여하는 효소의 누출 억제효과가 있는 것으로 사료된다. HPLC로 간 조직에서의 GSH측정결과t-BHP만 투여한 군과 비교하였을 때 유의적으로 증가하였고 조직학적 검사 결과 t-BHP만 투여한 군과 비교하였을 때 실크단백질 산 가수분해물을 투여한 군이 대조군과 가까운 모습을 보이는 것으로 관찰되어 실크단백질 산가수분해물이 산화적 스트레스로부터의 간 보호 효과가 있는 것으로 사료된다. 따라서 실크단백질 산 가수분해물의 기능적 소재로서의 이용가능성이 확대될 것으로 사료된다.

Background: This study was performed to evaluate the protective effect of Saururus chinensis ethanol extract (SCE) against styrene toxicity in mouse spermatocyte cells [GC-2spd (ts) cell line]. Methods and Results: Cytotoxicity in mouse spermatocyte cells was measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Generation of reactive oxygen species (ROS) was determined using 2’,7’-dichlorodihydrofluorescein diacetate (DCF-DA) assay. Semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and western blotting were performed to quantify the mRNA and protein expression levels, resepectiviely, of stress or apoptosis-related genes including p21, p53, heat shock protein 70 (Hsp70), heat shock protein 90 (Hsp90), Bax, Bcl-2, and caspase-3. The results of the MTT assay showed that 50 ㎍/㎖ SCE did not affect cell viability. ROS generation in mouse spermatocyte cells increased by treatment with 100 μM styrene, and decreased by co-treatment with SCE. SCE repressed the mRNA expression of stress-related genes, which increased by styrene treatment. In addition, SCE inhibited the apoptosis of mouse spermatocyte cells by ameliorating mRNA and protein levels of apoptotic genes that were altered by styrene treatment. Conclusions: These results suggest that SCE may alleviate styrene toxicity in mouse spermatocyte cells by reducing ROS stress and regulating genes related to styrene toxicity.

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 : 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.

It is difficult to predict scabbing limit thickness of fiber reinforced concrete, because existing formulas are not consider fiber reinforcing effect. So, In this study, obtaining the fiber reinforced factor and factors are applied to Modified NDRC formula. As results, it was possible to make accurate prediction for scabbing limit thickness of fiber reinforced concrete.

We investigated the antioxidative and protective effects of corn silk (Zea mays L.) ethanol extracts on human HaCaT cells and erythrocytes. The NICS-2 fraction, extracted from corn silk, exhibited favorable 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2-azino-bis-(3-ethylbenzothiazoline-6-sulphonic acid (ABTS) radical scavenging activities with IC50valuesof13.3± 0.3 μg/mL and 14.2 ± 0.1 μg/mL when compared with those of α-tocopherol, a positive control, with IC50=10.4± 02.2 and 22.2 ± 3.6 μg/mL, respectively. In addition, we investigated skin protection effects of NICS extracts of corn silk in HaCaT keratinocytes. To investigate the pharmacological potential of NICS-1 and NICS-2 extracts of corn silk on UV-B-induced damage in HaCaT cells, we measured the activity of interleukin (IL) 1a. Our results showed that all the corn silk extracts inhibited the UV-B-induced activity of IL-1a. In particular, NICS-1 extracts of corn silk significantly suppressed IL-1a activity in a dose-dependent manner without inducing cytotoxicity. These results indicate that the ethanol extracts of corn silk (Zea mays L.) could function as natural cytoprotective agents and antioxidants in biological systems, particularly the skin exposed to UV radiation, by protecting cellular membrane against reactive oxygen species (ROS).

본 연구에서는 드럼스틱 잎 추출물과 분획들의 항산화 활성 및 HaCaT 세포와 적혈구 세포에서의 세포보 호효과를 측정하였다. 모든 실험은 드럼스틱 잎의 50% 에탄올 추출물, 에틸아세테이트 분획 및 아글리콘 분획 을 이용하였다. 1,1-Diphenyl-2–picrylhydrazyl radical을 이용한 자유 라디칼 소거 활성(FSC50)은 50% 에 탄올 추출물(77.10 μ g/mL) < 에틸아세테이트 분획(20.63 μ g/mL) < 아글리콘 분획(17.00 μ g/mL) 순으로 증가하였다. 루미놀을 이용한 Fe3+-EDTA/H2O2계에서의 활성산소 소거 활성(총항산화능, OSC50)은 아글리콘 분획의 OSC50 값이 0.63 μ g/mL로 추출물 중 가장 큰 항산화능이 나타났으며, 이는 L-ascorbic acid (1.50 μ g/mL)의 항산화 활성보다 컸다. 1O2로 유도된 적혈구 세포 손상에 있어서 50% 에탄올 추출물 및 아글리콘 분획의 세포 보호 효과(τ50)는 10 μ g/mL에서 각각 46.9 및 122.1 min을 나타냈다. 이는 지용성 항산화제로 알려진 (+)-α-tocopherol (37.7 min)보다도 훨씬 큰 세포 보호 활성을 보여주었다. 400 mJ/cm2의 UVB를 HaCaT 세포에 조사하여 세포손상을 유도한 후 에틸아세테이트 분획 및 아글리콘 분획은 0.20 ∼ 1.56 μ g/mL 농도에서 농도 의존적으로 세포보호효과를 나타내었다. 이상의 결과들은 자외선에 노출된 피부에서 드럼스틱 잎 추출물과 분획들이 ROS 소거를 통하여 세포를 보호함으로서 화장품에서 천연 항산화제로서 사용 가능함을 시사하였다.

DJ#3과 DJ#13은 항염증질환 소재로서 가능성을 확인하 고자 국내 전통식품 풀질인증 된장에서 장기간 숙성된장으 로 선발된 시료이다. DJ#3과 DJ#13 추출물의 세포독성을 살펴보기 위하여 혈관내피세포를 이용하여 세포의 생존율 을 살펴본 결과 DJ#3과 DJ#13 추출물 모두 100 μg/mL의 농도까지 전혀 독성을 나타내지 않았다. 또한 DJ#3과 DJ#13 추출물의 항염증 효과를 TNF-α에 의해 활성화된 혈관내피세포에서의 NO 생성, 염증관련 단백질 발현과 mRNA 유전자 발현의 변화를 통하여 확인하였다. 혈관내 피세포에 TNF-α를 처리한 결과 NO의 함량이 유의적으로 감소하였다가 DJ#3과 DJ#13 추출물(20, 50, 100 μg/mL)을 처리하였을 때 유의성은 없으나 증가하였다. 세포배양액내 VCAM-1, ICAM-1 발현을 확인한 결과 혈관내피세포에 TNF-α를 처리한 군에서 증가된 VCAM-1 발현이 DJ#3 추출 물 20, 50 μg/mL에서 유의성 있는 감소를 보였다. 또한 DJ#3 추출물은 NO 생성과 연관 있는 eNOS mRNA의 발현을 농도 의존적으로 증가하였으며, iNOS mRNA의 발현은 농 도 의존적으로 감소하였으며 이는 NO 생성 증가가 iNOS의 발현억제를 경유한 것으로 사료된다. 또한 다수의 항염증 약물들의 작용기전이 되는 COX-2의 생성억제를 살펴본 결과 DJ#3 추출물은 TNF-α에 의해 발현되는 COX-2 단백질 의 발현을 억제하였음을 확인할 수 있었다. 또한, DJ#3 추출 물은 CAMs 단백질 및 mRNA 발현율의 감소됨을 보였다, 이상의 결과로 보아, DJ#3 추출물은 혈관내피세포에서 TNF-α로 유도된 혈관염증을 감소하는 효과를 가지고 있으 며, 항염증물질의 연구에 기초 자료로 활용이 가능할 것으 로 기대된다. 또한 염증과 관련된 cytokine 및 단백질 발현 메커니즘에 대한 추가적인 연구가 필요할 것으로 판단된다.

본 연구는 4종의 별의별간(SS) 음료의 간보호 소재로서 의 이용 가능성을 조사하고자 항산화능 평가, t-BHP 와 CCl4로 산화적 손상 및 급성 간독성 유도한in vitro, in vivo 모델을 활용하여 간보호능을 평가하였다. 실험결과, 별의별간 01~04는 50 μM vitamin C 와 유사한 항산화 효과를 나타내었다. HepG2 세포에 t-BHP로 산화 스트레스를 유도한 뒤 나타나는 세포독성에 대해 별의별간 01 및 04에서 농도 의존적인 세포 보호효과를 보였으며, ROS 생성 억제에서 별의별간 01, 03, 04에서 농도의존적인 억제를 나타내었다. 미나리가 혼합된 별의별간 04에 대한 급성 간손상in vivo 모델을 활용하여 간보호능 검증 결과, 별의별간 04는 CCl4로 증가된 혈중 ALT, AST의 유의적 감소, 간 조직중 증가된 MDA 함량 감소 및 감소된 GSH의 유의적 증가를 나타내었다. 또한, 혈청 및 간 조직에서 증가 된 중성지방과 콜레스테롤을 유의적으로 감소시켰다. 이러 한 결과를 종합하며, 별의별간 04는in vitro 및in vivo 모델 에서 산화적 손상에 대해 간보호 효과를 나타내었다

피부 손상은 주로 자외선, 열, 담배 등과 같은 환경적 요인으로부터 초래되는데, 이는 활성산소종의 과생 성으로 인한 피부노화와 연관이 있는 것으로 알려져 있다. 돌배(Pyrus pyrifolia NAKAI)는 전 세계적으로 많이 소비되는 과일로써 항암, 항산화, 항염증효과가 알려져 있다. 본 연구에서는 돌배나무잎 추출물(Pyrus pyrifolia leaf extract, PPE)의 ultraviolet B (UVB)스트레스에 대한 피부 섬유아세포 보호효과를 검증하였다. Lactate dehydrogenase assay와 DCF-DA를 이용한 정성분석 실험은 PPE가 인간의 섬유아세포에서 UVB 스트레스 에 의해 유발된 세포독성 및 과생성된 활성산소종을 농도 의존적으로 억제할 뿐만 아니라, 미토콘드리아 기능저 하, 막전위 저하, 그리고 세포사멸과정의 핵심 인자인 caspase-3 활성도 유의하게 억제함을 보여주었다. 결론적 으로, PPE는 UVB스트레스에 의해 과생성된 활성산소종을 억제시켰으며, 이로 인해 생기는 피부세포 사멸을 효과적으로 저해함을 확인하였다.

Pectin은 식물 세포벽의 주요성분으로 과실이나 채소류의 세포막이나 세포막 사이의 엷은 층에 존재하 며, 고점도의 수용성 다당체로 염과 pH에 의한 점도 변화가 심하며, 알코올류와 만나 gelation 되는 특징을 가 지고 있다. 식품분야에서 펙틴은 점도의 증가 및 겔 형성제로 사용되어 왔으나, 화장품 분야에서는 그 사용이 극히 제한적이었다. 본 연구에서는 pectin 효소 분해물의 분해 정도 및 분자량 분포를 정확히 확인하기 위해, HPLC (GPC)를 이용한 분석 조건을 확립하였으며, 생물 전환 공정을 통해 저분자량 pectin oligomer가 형성 되는 것을 확인하였다. 그리고, 2종의 효소에 대한 저분자량 pectin oligomer 생산 최적 조건 실험을 진행하여 최적 생산 조건을 확립하였으며, 이로 부터 제조한 pectin 효소분해물에서 저분자량 pectin oligomer를 선별적 으로 분리하는 공정도 개발하였다. 이러한 공정을 통해 제조된 저분자량 pectin oligomer 소재 LMPH A 와 B는 약 200 ∼ 2,700 Da 정도의 분자량 분포를 가지는 것으로 확인되었다. LMPH A와 B의 생리활성을 확인 한 결과, 2종 모두 항산화 활성을 보였다. 게다가, 이들이 pectin 및 D-galacturonic acid 보다 상대적으로 우 수하며, 농도의존적으로 증가함을 보였다. 또한 자외선(UVB)에 의한 피부세포의 광손상 및 이로 인한 apoptosis를 방어하는 효과를 나타내었다. 세포 활성화 효과 측정결과는 LMPH A, B 모두 0.025% 이상의 농도에 서 세포 활성화 효과를 보였으며, 농도가 0.5%에 이를 때까지 농도 의존적으로 증가하는 것을 확인할 수 있었 다. 특히, LMPH B의 경우, 0.5% 농도에서 약 30%, LMPH A도 약 22%의 매우 우수한 세포 활성화 효과를 가지는 것으로 확인되었다. 결론적으로, 본 연구를 통해 개발된 2종의 LMPH가 우수한 생리활성과 동시에 우수 한 안전성을 보임으로써, 향후 화장품 소재로 응용 가능성이 매우 높을 것으로 기대된다.

In this study, we investigated the anti oxidative potential and protective effects of water extract of Leonurus sibiricus L. leaf (LSLW) against ultraviolet B (UVB)-induced oxidative damage in human keratinocytes (HaCaT cells). To evaluate the anti oxidative activity of LSLW, we measured DPPH radical, hydroxyl radical, hydrogen peroxide, superoxide anion scavenging activities, lipid peroxidation inhibition, and reducing power of LSLW. For induction of oxidative stress in HaCaT cells, the cells were irradiated with UVB at 40 mJ/㎠. To investigate the protective effects of LSLW against UVB, we measured cell viability and apoptotic bodies using annexin V staining. LSLW showed anti oxidative activities by scavenging DPPH radical, hydroxyl radical, hydrogen peroxide, superoxide anion and by reducing lipid peroxidation. In addition, LSLW showed high reducing values. The UVB-induced oxidative conditions led to cell apoptosis. However, treatment with LSLW ameliorated oxidative stress conditions, including inhibition of cell death, apoptotic body. Taken together, LSLW exhibited anti oxidative and protective effects against UVB-induced damage in HaCaT cells. Thus, LSLW could be useful for the development of cosmetics for UVB-induced skin aging.

β amyloid protein (Aβ) plays a critical role in the pathogenesis of Alzheimer's disease (AD) and possibly in Aβ -induced mitochondrial dysfunction and oxidative stress. Aβ can directly cause reactive oxygen species (ROS) production. Overproduction of ROS is considered to be involved in the pathogenesis of neurodegeneration of AD. Here, we investigated 9 kinds of ramie (Boehmeria nivea, (L.) Gaud., BN; hereafter denoted as BN) for their protective action against oxidative stress in a cellular system using C6 glial cells. We observed loss of cell viability and high levels of ROS generation after treatment with hydrogen peroxide (H2O2) and Aβ25-35. However, treatments with BN extracts led to an increase in cell viability and decrease in ROS production induced by H2O2 and Aβ25-35. In particular, the extracts of BN-01 (seobang variety from Seocheon) and BN-09 (local variety from Yeonggwang) showed excellent anti-oxidative properties. This indicates that BN extracts could prevent neurodegeneration by reducing oxidative stress in cells.

오디 당침출액(MSE)의 산화적 스트레스 개선 효과를 확인하기 위하여 HepG2 세포에 H2O2로 산화적 스트레스를 유도시킨 다음, MSE의 보호효과를 확인하였다. MSE를 40 일간 저장하여 DPPH radical scavensing을 통해 DPPH radical 소거능이 유의적으로 좋았던 저장 40일용 MSE를 선택하여 세포 실험에 적용하였다. HepG2 세포에 500 μM H2O2를 처리하여 산화적 스트레스를 유발시키고, MSE를 처리하여 세포 생존율을 확인한 결과, MSE 처리로 인한 세포 생존율이 유의적으로 증가하였고, ROS 생성과 과산 화물에 대한 지표로 측정된 MDA 농도도 MSE 처리로 인해 효과적으로 억제되었다. 또한, H2O2 처리로 감소된 SOD 및 CAT 활성이 MSE 처리로 인해 유의적으로 높아졌으며, H2O2를 처리로 인한 세포핵의 apoptosis body가 MSE 처리 로 인해 감소함을 확인하였으며, 이는 caspase-3 활성 MSE 가 억제시킴으로 인해 세포를 보호하고 있음을 확인하였 다. 이상의 결과로부터 오디 당침출액은 산화적 스트레스 로부터 야기되는 세포독성과 apoptosis로부터 세포 보호 효과를 확인함에 따라 향후 노화와 관련된 다양한 연구 소재의 기초 자료 및 질병 예방 소재로의 가능성을 확인하 였다.

본 연구에서는 갈조류인 감태의 추출물과 그 분획들의 항산화 활성을 측정하였다. 모든 실험에서 감태의 50% 에탄올 추출물과 에틸아세테이트 분획, 아글리콘 분획을 사용하였다. DPPH (1,1-diphenyl-2-pic-rylhydrazyl)법을 이용한 자유 라디칼 소거 활성(FSC50)에서 에틸아세테이트 분획(FSC50 = 6.98 µg/mL)과 아글리콘 분획(7.03 µg/mL)은 비교물질인 (+)-α-tocopherol(8.98 µg/mL)과 유사한 활성을 나타냈다. 루미놀 발광법을 이용하여 Fe3+-EDTA/H2O2계에서 활성산소 소거 활성(총 항산화능, OSC50) 결과, 모든 추출물과 분획들 중에서 아글리콘 분획(OSC50 = 14.48 µg/mL)이 가장 큰 항산화능을 나타내었으나, 강력한 항산화제인 L-ascorbic acid (6.88 µg/mL)보다는 낮았다. 1O2로 유도된 사람 적혈구 세포 손상에 있어서 50% 에탄올 추출물은 5 ∼ 50 µg/mL에서 농도 의존적인 세포보호 효과를 나타냈다. 10 µg/mL에서 에틸아세테이트 분획과 아글리콘 분획의 세포보호 효과(τ50)는 각각 442.0 min 및 539.9 min으로 세포보호 활성이 크게 나타났다. 3종류의 감태 추출물 및 분획은 10 µg/mL에서, 비교물질인 지용성 항산화제 (+)-α-tocopherol (40.6 min)보다 훨씬 더 큰 세포보호 활성을 나타냈다. 이러한 결과들은 감태 추출물과 그 분획물들이 항노화 관련 화장품 분야에서 항산화제로서 이용 가능성이 있음을 시사하였다.