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마디풀(Polygonum aviculare L.) 추출물의 대식구 면역증강 효과
전창배,김영훈,Dulamjav Batsuren,Jigjidsuren Tunsag,노주원,판철호,이재권 대한약학회 2013 약학회지 Vol.57 No.6
In this study we demonstrated whether the extract of Polygonum aviculare L. (PAE) can be applied to the immune-stimulating responses in macrophages (Raw 264.7 cells). Cell viability was determined by WST-8 assay, and all four doses of PAE (5, 10, 20, and 40 µg/ml) had no significant cytotoxicity during the entire experimental period. PAE ncreased the production of inducible nitric oxide synthase (iNOS) and nitric oxide (NO), and mRNA expressions and protein levels of pro-inflammatory cytokines(tumor necrotic factor (TNF)-α, interleukin (IL)-1β and IL-6) in the same cells. These immune-stimulating activities of PAE were found to be caused by the stimulation of NFκB signal and phosphorylation of MAP kinases (p38, ERK and JNK).
A Fruit Extract of Paeonia anomala Attenuates Chronic Alcohol-induced Liver Damage in Rats
Sarangerel Oidovsambuu,윤지호,강경수,Batsuren Dulamjav,Jigjidsuren Tunsag,남의정,노주원 한국생약학회 2016 Natural Product Sciences Vol.22 No.4
Prolonged alcohol consumption causes alcoholic liver damage due to the generation of reactive oxygen species, the accumulation of fatty acids, and an increase in inflammatory cytokines in the liver. In this study, the protective effect of a fruit extract of Paeonia anomala (FEPA) against chronic alcohol-induced liver damage was evaluated in Sprague-Dawley rats fed an ethanol or a control Lieber-DeCarli diet for 5 weeks to induce alcoholic liver damage. FEPA (50, 25, and 10 mg/kg body weight/day) as well as the reference control silymarin (25 mg/kg body weight/day) were administered along with the ethanol diet. FEPA protected against increases in alanine aminotransferase and aspartate aminotransferase in serum and attenuated alcohol-induced increases in triglycerides, tumor necrosis factor alpha, thiobarbituric acid-reactive substances, and cytochrome P450 2E1 enzyme activity in the liver compared with the group treated with ethanol only. Anti-oxidative defenses such as the total glutathione level and glutathione peroxidase activity were increased by FEPA treatment. These results suggest that FEPA exerts protective effects against chronic alcohol-induced liver damage by attenuating hepatosteatosis and pro-inflammatory cytokine production and enhancing anti-oxidative defense mechanisms in the liver.
김영훈 ( Young Hoon Kim ),박은규 ( Eun Gyu Park ),( Dulamjav Batsuren ),( Jamsranjav Ganbaatar ),노주원 ( Chu Won Nho ),판철호 ( Cheol Ho Pan ),이재권 ( Jae Kwon Lee ) 한국응용생명화학회(구 한국농화학회) 2014 Journal of Applied Biological Chemistry (J. Appl. Vol.57 No.4
본 연구에서는 아직 까지 연구되지 않은 말굽버섯의 면역증강 효과를 설치류 대식세포에서 검증하였다. 연구결과에 따르면 말굽버섯 메탄올 추출물(FFE)의 처리에 의해 대식세포의 산화질소의 생성이 농도 의존적으로 증가되었다. 산화질소의 생성이 증가된 이유는 산호질소의 생성을 유도하는 효소인 iNOS의 발현이 FFE에 의해 증가되었기 때문이었다. FFE는 면역반응에 중요한 cytokine인 TNF-α, IL-1β, IL-6의 생성도 농도 의존적으로 증가 시켰다. 이 같은 FFE의 면역증강 활성은 면역활성을 중계하는 세포 신호전달분자 중 NF-κB와 MAP Kinases의 활성증가에 의한 것임을 확인 할 수 있었다. 본 연구 결과는 말굽버섯의 임상적 적용에 중요한 자료로 활용될 것이며, 만일 말굽버섯으로부터 분리한 단일성분에서 면역증강활성을 검증 하게 된다면 새로운 식·의약소재로서의 가치를 인정 받을 수 있을 것으로 생각된다. In this study, we demonstrated whether the extract of Fomes fomentarius (FFE; FF extract) could be used to stimulate macrophages (RAW 264.7 cells). All four doses of FFE (5, 10, 20, and 40 μg/mL) had no significant cytotoxicity during the entire experimental period. FFE potently increased the production of nitric oxide (NO). Consistent with these observations, inducible NO synthase levels were increased by FFE in a dose-dependent manner. Moreover, FFE increased the production of tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 in the same cells. These stimulating effects of FFE were found to be caused by the stimulation of phosphorylation of IκBα and MAP kinases (p38,ERK, and JNK). These results suggest that FFE may be used as new agents for wide application in the immune study of mushroom.
Kang, Kyungsu,Lee, Hee Ju,Kim, Chul Young,Lee, Saet Byoul,Tunsag, Jigjidsuren,Batsuren, Dulamjav,Nho, Chu Won Pharmaceutical Society of Japan 2007 BIOLOGICAL & PHARMACEUTICAL BULLETIN Vol.30 No.12
<P>The ethanol extract of the aerial part of the Mongolian medicinal plant <I>Saussurea salicifolia</I> induced a dose-dependent cell growth inhibition in both human gastric adenocarcinoma AGS cells and mouse hepatoma Hepa 1c1c7 cells (IC<SUB>50</SUB>=30.22 and 116.96 μg/ml), respectively. The extract induced an apoptosis in AGS cells inference from the externalization of the phosphatidylserine, the increase of the sub G0/G1 content (%) and the apoptotic morphological changes including membrane blebbing, the formation of apoptotic bodies and chromatin condensation. In order to identify active substances causing the apoptosis, we further isolated major compounds present in <I>Saussurea salicifolia</I> and 7 compounds were isolated including a sesquiterpene lactone, cynaropicrin, 3 lignans (trachelogenin, matairesinol and arctigenin) and 3 lignan glycosides (tracheloside, matairesinoside and arctiin). In general the lignan aglycones were more cytotoxic than their lignan glycosides in both AGS cells and Hepa 1c1c7 cells. Cynaropicrin not only showed the most potent cytotoxicity among the 7 major compounds but also it induced an apoptosis and a weak G2/M arrest in AGS cells. Arctigenin had the second-best cytotoxicity among 7 major compounds, and induced an apoptosis. In order to evaluate the induction of the phase II detoxification enzyme, we measured the induction of quinone reductase activity of the extract, fractions and compounds in Hepa 1c1c7 cells. The ethyl acetate fraction and arctigenin showed the strongest cancer chemopreventive activity (chemoprevention index=9.88 and 7.57, respectively). These data suggest that the extract as well as the lignan compounds (especially arctigenin) originated from <I>Saussurea salicifolia</I> may be served as potential cancer chemopreventive agents for prevention or treatment of human cancers.</P>
Kang, Kyungsu,Oh, Seung Hyun,Yun, Ji Ho,Jho, Eun Hye,Kang, Ju-Hee,Batsuren, Dulamjav,Tunsag, Jigjidsuren,Park, Kwang Hwa,Kim, Minkyun,Nho, Chu Won Elsevier 2011 Neoplasia Vol.13 No.11
<P>We report that daurinol, a novel arylnaphthalene lignan, is a promising potential anticancer agent with adverse effects that are less severe than those of etoposide, a clinical anticancer agent. Despite its potent antitumor activity, clinical use of etoposide is limited because of its adverse effects, including myelosuppression and the development of secondary leukemia. Here, we comprehensively compared the mechanistic differences between daurinol and etoposide because they have similar chemical structures. Etoposide, a topoisomerase II poison, is known to attenuate cancer cell proliferation through the inhibition of DNA synthesis. Etoposide treatment induces G(2)/M arrest, severe DNA damage, and the formation of giant nuclei in HCT116 cells. We hypothesized that the induction of DNA damage and nuclear enlargement due to abnormal chromosomal conditions could give rise to genomic instability in both tumor cells and in actively dividing normal cells, resulting in the toxic adverse effects of etoposide. We found that daurinol is a catalytic inhibitor of human topoisomerase Il alpha, and it induces S-phase arrest through the enhanced expression of cyclins E and A and by activation of the ATM/Chk/Cdc25A pathway in HCT116 cells. However, daurinol treatment did not cause DNA damage or nuclear enlargement in vitro. Finally, we confirmed the in vivo antitumor effects and adverse effects of daurinol and etoposide in nude mice xenograft models. Daurinol displayed potent antitumor effects without any significant loss of body weight or changes in hematological parameters, whereas etoposide treatment led to decreased body weight and white blood cell, red blood cell, and hemoglobin concentration.</P>