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Effects of epigallocatechin gallate on CoCl_(2)-induced apoptosis in PC12 cells
Yang, Kyu-Ho,Mo, Hyun-Chul,Choi, Nam-Ki,Kim, Seon-Mi,Kim,Won-Jae 大韓小兒齒科學會 2006 大韓小兒齒科學會誌 Vol.33 No.1
Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride (CoCl_(2)) has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG). a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by CoCl_(2) and effects of EGCG on CoCl_(2)-induced apoptosis in PC12 cells. Administration of CoCl_(2) decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with 100 µM EGCG for 30 min before PC12 cells were exposed to 150 µM CoCl_(2), being resulted in the cell viability and DNA fragmentation being rescued. CoCl_(2) caused morphologic changes such as cell swelling and condensed nuclei, whereas EGCG attenuated morphologic changes by CoCl_(2). EGCG suppressed the apoptotic peak and a loss of Δψ_(m) induced by CoCl_(2). CoCl_(2) decreased Bcl-2 expression but Bax expression was not changed in CoCl_(2)-treated cells. EGCG attenuated the Bcl-2 underexpression by CoCl_(2). CoCl_(2) augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity, a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by CoCl_(2). NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated CoCl_(2)-induced apoptosis in consistent with those of EGCG. These results suggest, that CoCl_(2) induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against CoCl_(2)-induced apoptosis in PC12 cells. 신경세포자멸사는 저산소 및 허혈환경에서 일어나며 이러한 세포죽은 reactive oxidant species (ROS) 생성을 동반함이 알려져있다. 그러나, 저산소 및 허혈환경에서 일어나는 세포자멸사의 기전 및 그 치료방법은 아직 정립되어 있지 않다. CoCl_(2)는 ROS를 생성하는 등 저산소환경과 유사한 조건을 초래하는 것으로 알려져 있다. Epigallocatechin gallate (EGCG)는 녹차의 polyphenol 성분으로서 세포성장과 죽음에 다양한 약리학적 효과를 나타냄이 알려져 있다. 본 연구는 PC12 세포에서 CoCl_(2)에 의한 세포자멸사기전을 밝히고 이에 미치는 EGCG의 효과를 조사하는데 목적이 있다. Cell viability는 MTT 측정으로 조사되었고, DNA fragmentation은 DNA laddering으로 조사되었다. Bcl-2와 Bax발현 정도는 RT-PCR로, caspase-3와 -9의 활성은 spectrophotometer, caspase-8의 활성은 flow cytometry에 의해 측정되었다. 미토콘드리아에서 세포질로 분비된 cytochrome c는 western blot으로, 분해된 DNA 양과 미토콘드리아 세포막전위 (Δψ_(m))는 FACScan으로 조사되었다. CoCl_(2)투여로 PC12 세포수는 용량 및 시간 의존형태로 감소하였고, genomic DNA fragmentation이 발생하였다. CoCl_(2)투여로 야기된 cell viability의 감소와 DNA fragmentation은 EGCG 전처치에 의해 억제되었다. CoCl_(2)은 세포용적팽창과 condensed nuclei 같은 형태적 변화를 일으켰으며, apoptotic peak, Δψ_(m)감소 및 cytochrome c 유리를 야기하였다. EGCG는 CoCl_(2)에 의한 세포형태변화, apoptotic peak, Δψ_(m)소실 및 cytochrome c 유리를 억제시켰다. CoCl_(2)는 Bcl-2 발현을 감소시켰지만, Bax 발현에는 영향을 미치지 않았다. EGCG는 CoCl_(2)에 의해 야기된 Bcl-2 발현 감소를 억제시켰다. CoCl_(2)는 caspase-3, -8, 그리고 -9의 활성을 증가시켰으며, EGCG는 CoCl_(2)에 의한 세포자멸사를 억제시켰다. 본 실험결과는 PC12 세포에서 CoCl_(2)가 미토콘드리아 의존 및 death receptor의존 기전으로 세포자멸사를 일으키며, EGCG는 세포자멸사기전을 억세지킴으로 신경보호기능을 가짐을 시사하였다.
키넥트 센서를 이용한 고령자 대상의 선자세 균형능력 평가
양승태(Seung-Tae Yang),강동원(Dong-Won Kang),서정우(Jeong-Woo Seo),김대혁(Dae-Hyeok Kim),김태호(Tae-Ho Kim),최진승(Jin-Seung Choi),탁계래(Gye-Rae Tack) 대한전기학회 2017 전기학회논문지 Vol.66 No.2
Portable low-cost Kinect sensor was used to analyze standing balance ability of the elderly. Eighty subjects who can walk alone and have a normal cognitive level participated in this experiment. Based on Berg Balance scale (BBS) test with 52 points, subjects were divided into Healthy older (HO: 46 persons, BBS: 53.80 ± 1.19) and Impaired older (IO: 34 persons, BBS: 49.06 ± 2.03) group. Each subject performed 30 seconds four different standing balance tests (EO: Eyes Open, EC: Eyes Close, EOf: Eyes Open on foam, ECf: Eyes Close on foam). Five variables (Mean distance, Range of distance, Root mean square, Mean velocity, 95% ellipse area) were calculated from the hip joint center movement of Kinect sensor. Results showed that there were significant differences between groups for four different standing tests. Calculated variables from kinect sensor showed significant correlation with BBS score. Especially, mediolateral mean distance, mediolateral root mean square, mediolateral range of distance and 95% ellipse area showed discriminative ability for all tests. Mean values of variables of IO were higher than those of HO, which means the decreased balance ability in IO compared with HO. Therefore, it was possible to estimate simple balance assessment of the elderly using portable low-cost Kinect sensor.
Yang, Keum-Jin,Shin, Sanghee,Piao, Longzhen,Shin, Eulsoon,Li, Yuwen,Park, Kyeong Ah,Byun, Hee Sun,Won, Minho,Hong, Janghee,Kweon, Gi Ryang,Hur, Gang Min,Seok, Jeong Ho,Chun, Taehoon,Brazil, Derek P,He American Society for Biochemistry and Molecular Bi 2008 The Journal of biological chemistry Vol.283 No.3
<P>3-Phosphoinositide-dependent protein kinase-1 (PDK1) appears to play a central regulatory role in many cell signalings between phosphoinositide-3 kinase and various intracellular serine/threonine kinases. In resting cells, PDK1 is known to be constitutively active and is further activated by tyrosine phosphorylation (Tyr(9) and Tyr(373/376)) following the treatment of the cell with insulin or pervanadate. However, little is known about the mechanisms for this additional activation of PDK1. Here, we report that the SH2 domain of Src, Crk, and GAP recognized tyrosine-phosphorylated PDK1 in vitro. Destabilization of PDK1 induced by geldanamycin (a Hsp90 inhibitor) was partially blocked in HEK 293 cells expressing PDK1-Y9F. Co-expression of Hsp90 enhanced PDK1-Src complex formation and led to further increased PDK1 activity toward PKB and SGK. Immunohistochemical analysis with anti-phospho-Tyr(9) antibodies showed that the level of Tyr(9) phosphorylation was markedly increased in tumor samples compared with normal. Taken together, these data suggest that phosphorylation of PDK1 on Tyr(9), distinct from Tyr(373/376), is important for PDK1/Src complex formation, leading to PDK1 activation. Furthermore, Tyr(9) phosphorylation is critical for the stabilization of both PDK1 and the PDK1/Src complex via Hsp90-mediated protection of PDK1 degradation.</P>
Won, Jong-Heon,Im, Ho-Teak,Kim, Yang-Hee,Yun, Kyung-Jin,Park, Hee-Juhn,Choi, Jong-Won,Lee, Kyung-Tae 경희대학교 동서의학연구소 2006 東西醫學硏究所 論文集 Vol.2006 No.-
1 Buddlejasaponin IV isolated from Pleurospermum kamtschatidum is an anti-inflammatory compound that inhibits NO, PGE_(2) and TNF-α. production. Here, we studied the mode of action of this compound. 2 Buddlejasaponin IV (2.5-10μm) reduced lipopolysaccaride (LPS (1 μg ml^(-1)))-induced levels of iNOS and COX-2 at the protein levels, and iNOS, COX-2, TNF-α, interleukin (IL)-1β and IL-6 mRNA expression in RAW 264.7 macrophages in a concentration-dependent manner, as determined by Western blotting and RT-PCR, respectively. 3 Buddlejasaponin IV inhibited the LPS-induced activation of nuclear factor-KB (NF-κB), a transcription factor necessary for proinflammatory mediators, iNOS, COX-2, TNF-α, IL-1β and IL-6 expression. This effect was accompanied by a parallel reduction in IkB-α degradation and phosphorylation, and by the nuclear translocation of the NF-κB p65 subunit. 4 The effects of buddlejasaponin IV on acute phase inflammation were studied on serotonin- and carrageenan-induced paw edema. The antiedematous effect of buddlejasaponin IV was compared with 10 mgkg^(-1) of indomethacin p.o. Maximum inhibitions of 26 and 41% were noted at a dose of 20 mgkg^(-1) for serotonin- and carrageenan-induced paw edema, respectively. 5 The analgesic effect of buddlejasaponin IV was evaluated using acetic acid-induced writhing and hot-plate tests. Buddlejasaponin IV (10 and 20 mgkg^(-1), p.o.) was found to have a marked analgesic effect in both models. 6 These results suggest that the inhibitions of the expressions of iNOS, COX-2, TNF-α, IL-1β and IL-6 by blocking NF-κB activation, are responsible for the anti-inflammatory effects of buddlejasaponin IV isolated from P. kamtschatidum.
The Short Channel Effect Immunity of Silicon Nanowire SONOS Flash Memory Using TCAD Simulation
Yang, Seung-Dong,Oh, Jae-Sub,Yun, Ho-Jin,Jeong, Kwang-Seok,Kim, Yu-Mi,Lee, Sang Youl,Lee, Hi-Deok,Lee, Ga-Won The Korean Institute of Electrical and Electronic 2013 Transactions on Electrical and Electronic Material Vol.14 No.3
Silicon nanowire (SiNW) silicon-oxide-nitride-oxide-silicon (SONOS) flash memory devices were fabricated and their electrical characteristics were analyzed. Compared to planar SONOS devices, these SiNW SONOS devices have good program/erase (P/E) characteristics and a large threshold voltage ($V_T$) shift of 2.5 V in 1ms using a gate pulse of +14 V. The devices also show excellent immunity to short channel effects (SCEs) due to enhanced gate controllability, which becomes more apparent as the nanowire width decreases. This is attributed to the fully depleted mode operation as the nanowire becomes narrower. 3D TCAD simulations of both devices show that the electric field of the junction area is significantly reduced in the SiNW structure.