Photodynamic therapy(PDT) 는 특정 광 감응 물질 에 광 조사를 수행하여 세 포내애서 활성 산소종(ROS) 의 증가를 통한 암세 포의 사띨을 유도하는 방법이다 광 감응 물질은 암세 포에 선택 적으로 흡수되어 특정 파장의 빛을 홉수하여 다량의 ROS를 발생하여 암세 포의 사멸을 유도한다， 그러나 PDT 수행 시 ROS의 세 포내 작용에 따른 사띨 기전 이 영확히 알려지 지 않았고， 비 선 택 성으로 인한 정 상 세포애서의 피해 도 유발될 수 있다고 보고되었다 본 연 구애서 는 굉 감웅제인 He ma to por p h y rin을 이 용하여 구깅암 세포주인 He p2에서 광조사를 통한 세포 사멸 에 관한 연 구를 수행하였다 Confocal mi crosco py를 통한 분석에서 Hemato po r phyrin은 홉수 시 간에 따라 세포막에서 세 포질 핵 으로의 위치함을 관찰 할 수 있었고. 전기 영 동에 따른 DNA 분절 분석에서 24 시간이상 홉수된 상태 에서 ladder 패턴을 보임으로써 세 포 자띨사에 이 르는 만웅을 보였다 DCF - DA에 의힌 세 포내 ROS 분석 을 수행힌 결과 Hema to po rphyrin의 흡수 시간이 증가할수록 세포 내부에서의 ROS 발생이 증가함을 획 인 할 수 있었 다 이와 같은 결과에 따르면 Hematoporphyrin을 이용한 PDT에서 h ematoporphy ri n의 홉수 시 간에 따라 세 포 자띨사가 유도되었고. 특히 Hematoporphyrin은 흡수 시 간이 증가하여 세 포 내 부까지 충분히 Hematoporphyri n 이 작용된 경우에 서 ‘ ROS 발생애 따른 미 토콘드리아 의존적 경 로를 통해 세 포 자멸사가 유도되 었음을 확인 할 수 있었다-

Glycyrrhiza ura lensis (Leguminosae) has long been known as an ant i-i nflammatory agent for gastric 띠cers ， arthri t is, and rheumaLism. 1'he f1avonoid glycyr ol isolated from Glycyrrhiza uralensis dramatically inhibits phorbol ester (PMA)-induced NF-kB-dependent transcriptional activity, as determined by luciferase activity in HEK293T cells To in vestigate the global gene expression profiling by glycyrol, we performed high-density oligonucleotide microarrays, Our microarray analysis showed that gl ycY I 이 inhi bited phorbol ester-induced NF-kB-dependent transcriptional activity in inflarnmatory-related gene expression, RT-PCR analysis based on microarry data showed that NF-kB-dependent genes such as CCL2‘ CCL7. CD44, and HSPB8 in addition to NF-kB itself were significantly down-regulated by glycyrol Treatment with glycyrol inhibited ]-kB degradation induced by PMA, suggesting that glycyrol has a potential anti-in flammatory activity by modulating NF-kB-dependent pathways. Also, the microarray data showed that glycyr이 appears to induce gene expression related to p53-dependent apoptosis t hrough ENDO G instead of CAD/DFF and AlF/PDCD8 as down stream apoptosis factor in HEK293T tumor cell s and to induce an added function as oncogenes in connection with apoptoslS

The nitric oxide(NO) is a major factor contri buting to t he loss of neurons in ischemic st roke. demyelina t ing diseases, and other neurodegenerative di sorders . But it is known that NO is not function ing as a direct neurotoxin. NO combined with superoxide(02-) by the diffusion-contl'O ll ed reaction, formed a peroxin it ri te anion (ONOO-)‘ which this s pecies has been shown to contribute to oxidative s igna ling and damage. ONOO stimuJates apoptosis in many cell types. whether ONOO acts direct ly as an ox idant 0 1' the induction of apoptosis is because of the radicals derived from ONOO- decompositi on . But. the mecha ni sm by which ONOO- induces apoptosis is un clear although subsequent forrnation 0 1' reactive oxygen s pecies(ROS) has been suggested in a few reports The aim of this study is to investigate the a nti -apoptotic pathway by inhibi tion 0 1' ONOO synthesis t hrough scavenging of ROS us ing s pecific wavelength 0 1' light irradiation . The present study investi gated the a nti -apop totic effect of the specific wavelength 0 1' irradi ation in Sodium Nitroprusside(SNP) t reated SJ-I-SY5Y ceJls, by MTT, DNA fragmentation, and flow cytometric assay and th rough western blot and caspase-3, -9 activity assay for confirmation of caspase pathway. Also. NO reJease and ROS leveJ was measured in order to observe the changes of NO involved in radical by Griess reaction analysis and DCF'-DH. Results showed that the cell viability were r educed by about 50% of control group by SNP treatment, but re covered to about 80% by 590nm irradiation . The apoptotic cells were observed by flow cytomet ry and DNA fra g mentation assay in SNP-treated group‘ but 590nm irradiation led apoptotic feature to be reduced . Released NO a nd ROS level were increased after SNP treatment but ROS level was dec reased in 590nm irradi at ion - treated group, in spite of high NO concentration fo llowing SNP treatment Also. SNP t reatment led cytochrom C release but 590nm irraidiation inhibit it, hence the expression 0 1' caspase-3 and -9 was dec reased sign ificantly‘ These results showed that 590nm irradiation protect neuronal death thl'Ough bl ocking of NO-induced mi tochondri al apoptotic pathway. Also, it suggests that specific wavelength of irradi ation was used for prevent ion from neurodegenerative disordcr progression

It has been reported that light-emitting diodes(LED) can be used in the treatment of oral diseases. Although bio-stimulatory effects of LED irradiation such as promotes stimulation of wound healing have been well known, there are few reports about molecular mechanism associated with cell cycle by LED irradiation. The purpose of present study was to examine the molecular event in cell cycle of LED irradiation on primary human gingival fibroblast(hGF) in vitro. The source of light for irradiation was a continuous-wave LED emitting at a wavelength of 635nm, and manufactured that energy density was 5mW/cm2 on sample surface. The hGF were irradiated for 1 hour at 37℃ in 5% CO2 humidified chamber. Experimental samples were acquired at 0 (right after irradiation), 8 and 24 hour after irradiation. To investigate the molecular mechanisms associated with cell cycle, growth phase was determined by flow cytometry and mRNA expression of cyclin A, cyclin B, cyclin D1, cyclin E, cdc2, PCNA, p18, p27, p21, and p53 were determined by real time RT-PCR. Flow cytometric analysis demonstrated the percentage of cells in the G1 and S phase were decreased, but the G2 phase increased, which showed cells irradiated by LED were transitioned from S to G2 phase. For mRNA expression, cyclin B, cdc2, PCNA and p53 were increased at 0 hour after irradiation, and most of cell cycle molecules were increased at 8 hour after irradiation. At 24 hour after irradiation, cyclin A, cyclin E, PCNA and p18 were increased. Taken together, LED irradiation induced proliferation of hGF cells through transition from S to G2 phase.

The purpose 01' pl'esent study was to examine the molecular events in apoptosis by CoCl2, mimicking hypoxic cond ition and recovering effects by LED ir l'adiation on Human SH-SY5Y neuroblastoma cells The SOUl'ce 0 1' light for ir l'adiation was a continuous-wave LED emitting at a wavelenl양h of 590 nm, and manufactured that ene rgy density was 5 mW!cm2 on sample surface, After ir l'adiation, cell viabi lity was measured with BrdU , cell morphol ogy was examined with Diff- Quik staining, cell signaling was monitored with various apoptosis-related molecules using RNase Pl'otection Assay(RPA) , W11en treated with CoC12, apoptotic induction was found in the SH-SY5Y cells in a concentration-dependent and time-dependent manner , Diff-Quik s taining was revealed that DNA fragmentation re presented apoptosis was examined in CoC12-tl'eated group, Moreover, RPA assay of SH-SY5Y cclls lIs ing val'iolls apoptosis-related molecllles showed that the apoptotic cell population was mcreased J-loweve. there was sorne signifïcant change in LED irradiatied cells aftel' treatement of CoC12 The main mechanism for Lhese a poptosis appearecl to be mito c hondriεt - m ecliated pathway, such as cytochrome- c‘ caspase-9, caspase-3, pro-apototic protein ßax, anti-apototic protein Bcl-2, and death receptor• mediated pathway, such as Fas, cas pase- 8, a ncl TNFRl These results demonstrate that CoCI2 induce apoptosis in SH-SY5Y via different dual apop tosis pathway through death receptor pathway as well as mitochondria- dependent pathway and LED irradiation can recl llces the CoCl2-induced apoptosis by blocking their internal signaling pathway

μ방lt emitting diodes (LED) devices are commercially introduced as an alternative for low-Ievellaser therapy (11ι，T) ， and it has several advantages over lasers such as a safe, efficient, and less-expensive altemative to treat wounds. And LED irradiation at the same biostimulatory wavelength has similar bíochemical effεαs. In the present study, to asses whether the I핑ht-emitting diode (LED) irradíation can stimulate bone regeneration, irradiated bony defects with or without grafting materials on rat calvaria were compared to corresponding nonirradiated control. Fifty male Sprague-Dawly rats weighing about 150g, were used. Factors for present study were designed as follows, 1) presence or absence of grafting materials, 2) with or without irradiation, and 3) number of irradiation. Two weeks after operation, rats were sacrifìced. Radiologic and 비stomorphologic fmdings were evaluated. Macrospically, there were no incidents of infection, dehiscence, hematoma and necrosis during study. Radiological findings showed greater radiopacity in the graft group and radiopacity increased as the number of irradiation increase. And microscopically, new bαle formation was great in the graft group and increased as the number of irradiation increase, Present study has shown that LED irradiation improved bone regeneration through radiologic and histomorphologic fmdings in rat.