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송이 (Tricholoma matsutake) 자실체의 화학성분
이학주,최윤정,가강현,박원철 한국목재공학회 2003 목재공학 Vol.31 No.4
송이(Tricholoma matsutake) 자실체의 메탄올(methanol, MeOH) 추출물로부터 4개의 화합물을 분리하였으며, 기기분석 결과 adcnosinc (9-β-D-ribofuranosyladenine)을 비롯하여, methyl trans-cinnamate, ergosterol (ergosta-5, 7, 22-triene-3β-ol) 및 ergosta-4, 6, 8 (14), 22-tetraen-3-one으로 각각 동정하였다. One alkaloid derivatives, one amide and two steroids were isolated from the fruit bodies of Tricholoma matsutake. The structures were determinded as adenosine, methyl trans-cinnamate, ergosterol and ergosta-4, 6, 8 (14), 22-tetraen-3-one, respectively, on the basis of spectroscopic data.
Bak, Yesol,Kim, Heejong,Kang, Jeong-Woo,Lee, Dong Hun,Kim, Man Sub,Park, Yun Sun,Kim, Jung-Hee,Jung, Kang-Yeoun,Lim, Yoongho,Hong, Jintae,Yoon, Do-Young American Chemical Society 2011 Journal of agricultural and food chemistry Vol.59 No.18
<P>Naringenin, a well-known naturally occurring flavonone, demonstrates cytotoxicity in a variety of human cancer cell lines; its inhibitory effects on tumor growth have spurred interest in its therapeutic application. In this study, naringenin was derivatized to produce more effective small-molecule inhibitors of cancer cell proliferation, and the anticancer effects of its derivative, 5-hydroxy-7,4′-diacetyloxyflavanone-<I>N</I>-phenyl hydrazone (N101-43), in non-small-cell lung cancer (NSCLC) cell lines NCI-H460, A549, and NCI-H1299 were investigated. Naringenin itself possesses no cytotoxicity against lung cancer cells. In contrast, N101-43 inhibits proliferation of both NCI-H460 and A549 cell lines; this capacity is lost in p53-lacking NCI-H1299 cells. N101-43 induces apoptosis via sub-G<SUB>1</SUB> cell-cycle arrest in NCI-H460 and via G<SUB>0</SUB>/G<SUB>1</SUB> arrest in A549 cells. Expression of apoptosis and cell-cycle regulatory factors is altered: Cyclins A and D1 and phospho-pRb are down-regulated, but expression of CDK inhibitors such as p21, p27, and p53 is enhanced by N101-43 treatment; N101-43 also increases expression levels of the extrinsic death receptor Fas and its binding partner FasL. Furthermore, N101-43 treatment diminishes levels of cell survival factors such as PI3K and p-Akt dose-dependently, and N101-43 additionally induces cleavage of the pro-apoptotic factors caspase-3, caspase-8, and poly ADP-ribose polymerase (PARP). Cumulatively, these investigations show that the naringenin derivative N101-43 induces apoptosis via up-regulation of Fas/FasL expression, activation of caspase cascades, and inhibition of PI3K/Akt survival signaling pathways in NCI-H460 and A549 cells. In conclusion, these data indicate that N101-43 may have potential as an anticancer agent in NSCLC.</P>
Discrete-Time Sliding Mode Controller for Linear Time-Varying Systems with Disturbances
Park, Kang-Bak Institute of Control 2000 Transaction on control, automation and systems eng Vol.2 No.4
In this paper, a discrete-time sliding mode controller for linear time-varying systems with disturbances is proposed. The proposed method guarantees the systems state is globally uniformly ultimately bounded(G.U.U.B) under the existence of time-varying disturbances.
Seong Hee Kang,Dong-Ho Bak,Byung Yeoup Chung,Hyoung-Woo Bai,Bo Sun Kang 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.5
Delphinidin is a major anthocyanidin compound found in various vegetables and fruits. It has anti-oxidant, anti-inflammatory, and various other biological activities. In this study we demonstrated the anti-cancer activity of delphinidin, which was related to autophagy, in radiation-exposed non-small cell lung cancer (NSCLC). Radiosensitising effects were assessed in vitro by treating cells with a subcytotoxic dose of delphinidin (5 μM) before exposure to γ-ionising radiation (IR). We found that treatment with delphinidin or IR induced NSCLC cell death in vitro; however the combination of delphinidin pre-treatment and IR was more effective than either agent alone, yielding a radiation enhancement ratio of 1.54 at the 50% lethal dose. Moreover, combined treatment with delphinidin and IR, enhanced apoptotic cell death, suppressed the mTOR pathway, and activated the JNK/MAPK pathway. Delphinidin inhibited the phosphorylation of PI3K, AKT, and mTOR, and increased the expression of autophagy-induced cell death associated-protein in radiation-exposed NSCLC cells. In addition, JNK phosphorylation was upregulated by delphinidin pre-treatment in radiation-exposed NSCLC cells. Collectively, these results show that delphinidin acts as a radiation-sensitizing agent through autophagy induction and JNK/MAPK pathway activation, thus enhancing apoptotic cell death in NSCLC cells.