Ischemic stroke causes brain damage and neuronal cell death by depriving oxygen and nutrients and releasing excessive levels of glutamate and intracellular calcium. Epigallocatechin gallate (EGCG) is a polyphenolic compound present in green tea. It has antioxidant, anti-inflammatory, and neuroprotective effects. Hippocalcin is a calcium binding protein that regulates calcium concentration, neuronal differentiation, neuronal excitability, and neuronal cell death. In this study, we investigated whether EGCG regulates the expression of hippocalcin in neurons and astrocytes after focal cerebral ischemia. Cerebral ischemia was induced by meddle cerebral artery occlusion (MCAO). EGCG (50 mg/kg) or PBS was injected into the abdominal cavity just before MCAO surgery. Neurobehavioral tests were performed to evaluate the effect of EGCG on neurological behavioral deficits 24 h after MCAO surgery. Immunofluorescence staining was performed to evaluate the positive response to hippocalcin in the cerebral cortex after MCAO surgery. We also detected the positive reactions of neuronal nuclear protein (NeuN) and glial fibrillary acidic protein (GFAP) as markers of neuron and astrocyte, respectively. MCAO caused severe neurological impairment and EGCG treatment attenuated these impairments. MCAO damage reduced the number of NeuN-positive cells and increased the number of GFAP-positive cells. This result indicates a decrease in neurons and an increase in astrocytes. However, EGCG alleviated these changes caused by MCAO damage. MCAO reduced the number of hippocalcin-positive cells in neurons and astrocytes, and EGCG treatment attenuated these reductions. Hippocalcin exerts neuroprotective effect through regulating intracellular calcium concentration. In conclusion, EGCG regulates the expression of hippocalcin in neurons and astrocytes and has neuroprotective effects in focal cerebral ischemia.

Green tea polyphenol (–)-epigallocatechin-3-gallate (EGCG) is a potent antioxidant with protective effects against neurotoxicity. However, it is currently unclear whether EGCG protects neuronal cells against radiation-induced damage. Therefore, the objective of this study was to investigate the effects of EGCG on ultraviolet (UV)-induced oxidative stress and apoptosis in PC12 cells. The effects of UV irradiation included apoptotic cell death, which was associated with DNA fragmentation, reactive oxygen species (ROS) production, enhanced caspase-3 and caspase-9 activity, and poly (ADP-ribose) polymerase cleavage. UV irradiation also increased the Bax/Bcl-2 ratio and mitochondrial pathway-associated cytochrome c expression. However, pretreatment with EGCG before UV exposure markedly decreased UV-induced DNA fragmentation and ROS production. Furthermore, the UV irradiationinduced increase in Bax/Bcl-2 ratio, cytochrome c upregulation, and caspase-3 and caspase-9 activation were each ameliorated by EGCG pretreatment. Additionally, EGCG suppressed UV-induced phosphorylation of p38 and rescued UV-downregulated phosphorylation of ERK. Taken together, these results suggest that EGCG prevents UV irradiationinduced apoptosis in PC12 cells by scavenging ROS and inhibiting the mitochondrial pathways known to play a crucial role in apoptosis. In addition, EGCG inhibits UV-induced apoptosis via JNK inactivation and ERK activation in PC12 cells. Thus, EGCG represents a potential neuroprotective agent that could be applied to prevent neuronal cell death induced by UV irradiation.

목적: 항균제 polyhexamethylene Biguanide(PHMB), epigallocatechin gallate(EGCG) 및 PHMB/EGCG 혼합물의 각막상피세포(primary human corneal epithelial cells, HCEpiCs)에 대한 급성독성을 평가하고자 하였다. 방법: 각막상피세포를 0.00001~0.005% PHMB, 0.001~5% EGCG 및 0.00005% PHMB/0.05% EGCG 혼합물이 각각 포함된 배양액에서 30분, 60분, 120분 및 240분 동안 배양하였다. 배양한 각막상피세포를 고정한 다음 Draq 5로 염색하고 공초점현미경과 ImageXpress UltraTM를 이용하여 세포형태를 관찰하여 세포 생존율과 세포자살(apoptosis)을 비교하였다. 결과: 배양된 각막상피세포는 0.00005% 이하의 PHMB 농도 및 0.05% 이하의 EGCG 농도에서는 세포 독성이 나타나지 않았다. 0.00005% PHMB/0.05% EGCG 혼합물이 포함된 배양액에서 급성 세포독성은 관찰되지 않았으나 240분 배양시킨 경우에는 손상된 각막상피세포 수가 증가하고 생존 세포의 수는 감소하였다. 결론: 항균 시너지 효과를 갖는다고 보고된 0.00005% PHMB/0.05% EGCG 혼합물의 경우 각막상피세포에 대한 급성독성은 없었으나 만성효과에 대해서는 추가적인 연구가 필요할 것으로 생각된다.

(-)-Epigallocatechin-3-gallate (EGCG) is a major catechin found in green tea. It is reported that EGCG possesses various health benefits including anti-cancer, antioxidant, anti-diabetes, and anti-obesity. The objective of this study was to investigate the effects of EGCG on adipogenesis via activation of AMP-activated protein kinase (AMPK) pathway in 3T3-L1 preadipocytes. In order to determine the effects of EGCG on adipogenesis, preadipocyte differentiation was induced in the presence or absence of EGCG (0~100 μM) for a period of 6 days. EGCG significantly inhibited fat accumulation and suppressed the expression of adipogenic specific proteins including peroxisome proliferator-activated receptor (PPAR)-γ. Also, EGCG markedly increased the activation of AMPK and acetyl-CoA carboxylase (ACC) and the production of intracellular reactive oxygen species (ROS). However, any pretreatment with a specific AMPK inhibitor, compound C, abolished the inhibitory effects of the EGCG on PPARγ expression. This study suggests that EGCG has anti-adipogenic effects through modulation of the AMPK signaling pathway and therefore, may be a promising antiobesity agent.

Biofouling in brackish water reverse osmosis (RO) membranes still needs extensive research to understand cause and mechanism and to obtain methods for reduction of its impact on RO applications. Natural compounds with biofilm formation inhibitory properties are being investigated. Two compounds, vanillin and Epigallocatechin gallate (EGCG), were selected due to their great potential on biofilm formation inhibition. Vanillin shows inhibition on quorum sensing mechanisms of biofilm formation. EGCG has potential to inactivate microbial activity. The two compounds were incorporated in typical polyamide reverse osmosis membranes and evaluated on flux behaviours and biofilm formation potential. The surface properties of membrane coated with vanillin were changed tremendously compared to those with EGCG. As a result, the flux was reduced substantially. The biofilm formation seems hindered with EGCG coated membranes compared to the virgin membranes. More research is needed to optimize coating methods applicable to RO membranes and to enhance biofouling reduction.

목적: Polyhexamethylene biguanide (PHMB)와 Epigallocatechin-gallate (EGCG) 혼합물의 각막염 유발 균주에 대한 항균효과를 검사하고 콘택트렌즈 관리용액의 항균제로서의 가능성을 판단하고자 하였다. 방법: 국제표준화기구(International Organization for Standardization, ISO)가 규정한 황색포도상 구균(Staphylococcus aureus), 메티실린내성 황색포도상구균(Methicillin-resistant Staphylococcus aureus), 녹농균(Pseudomonas aeruginosa), 세라티아 마르세센스(Serratia marcescens), 칸디다 알비캔 스(Candida albicans), 푸사리움 솔라니(Fusarium solai)를 각각의 액체배지에 접종한 후 각 균주들의 적정 배양온도에서 24시간동안 활성화시켰다. 활성화된 균주는 96-well plate를 사용하여 PHMB와 EGCG를 각 각 0.0000125~0.0004%, 0.0025~0.3% 함유한 액체배지에서 배양하였고, PHMB/EGCG 혼합물은 PHMB 최소저해농도(MIC, 0.00005%)와 0.0125~0.1%의 EGCG가 포함되도록 하여 12시간 동안 배양하였다. 배양 후 항균력은 600nm에서 흡광도를 측정하여 확인하였다. 결과: ISO 규정 안질환 균주에 대한 EGCG 최소저해농도는 PHMB보다 높아(100~1,500배) 항균력은 낮은 것으로 평가되었다. PHMB/EGCG 혼합물의 ISO 규정 안질환 균주에 대한 최소저해농도는 0.00005%/ 0.05%로 PHMB 최소저해농도의 25% 수준에서도 충분한 항균효과를 나타내었다. 결론: PHMB와 EGCG 혼합물은 ISO 규정 안질환 균주에 대하여 항균 시너지 효과를 나타내어 다목적 용액에 사용하는 PHMB 농도를 낮출 수 있을 것으로 보이며 이 결과는 콘택트렌즈 관리용액 개발에 기초자료로 활용될 수 있을 것으로 사료된다.

Resveratrol (RVT) and epigallocatechin gallate (EGCG) individually inhibit adipogenesis in 3T3-L1 adipocytes. The objective was to examine the possibility of interaction between RVT and EGCG, resulting in enhanced inhibition of adipogenesis in 3T3-L1 adipocytes. Preadipocytes were treated with RVT and EGCG individually at 6.25 or 25μM (RVT6.25 or RVT25) and 12.5 or 50μM (EGCG12.5 or EGCG50) and in combination (RVT6.25 + EGCG12.5 and RVT25 + EGCG50). RVT25 as an individual compound decreased lipid accumulation in 3T3-L1 adipocytes by 24%, and RVT25 + EGCG50 further decreased lipid accumulation by 77%. In addition, exposure of 3T3-L1 adipocytes to RVT6.25 + EGCG12.5 and RVT25 + EGCG50 combinations resulted in an enhanced increase of adiponectin release and inhibition of leptin release. Quantitative analysis revealed that the combination of tested materials (RVT6.25 + EGCG12.5 and RVT25 + EGCG50) decreased the expression levels of C/EBPα, PPARγ2, and aP2. These results indicate that the combined treatments with RVT and EGCG produce synergistic effects on inhibiting adipogenesis in 3T3-L1 adipocytes. The overall results suggested that the combining RVT and EGCG might be more capable of exerting antiobesity effects than each individual compound by itself.

EGCG has inhibitory effect on a variety of cancers by inducing apoptosis and cell cycle arrest or inhibiting angiogenesis and metastasis. EGCG has been found to induce apoptosis in salivary gland carcinoma cells. But the potential anti-invasive effect of EGCG in salivary gland cancer has not been studied yet. The aim of this study is to evaluate the effect of EGCG on salivary gland adenocarcinoma SGT cell adhesion and migration to Type I collagen treatment. Western blot, adhesion and migration assay were performed to evaluate the impacts of EGCG on the expression of MMP-2/-9 and its upstream signaling molecules after treatment of type I collagen. SGT cell adhesion to type I collagen is significantly suppressed by EGCG. EGCG decreased expression of β1 integrin, phosphorylation of FAK, MMP-2/-9 compared with type I collagen treatment. In addition, EGCG inhibited the migration of SGT cells treated with type I collagen. These results suggest that EGCG could effectively inhibit the invasion and migration of human SGT cells by downregulating the expression of β1 integrin and MMP-2/-9 and phosphorylation of FAK, Akt, and Erk. Adhesion and migration to type I collagen of SGT cells can be influenced through EGCG.

Epigallocatechin-3-gallate (EGCG) and theaflavins (TF) are polyphenols included in green and black teas, respectively. Both green and black teas have been studied for their potential health benefits for cancer. Hypoxia-inducible factor (HIF) has been implicated multiple physiological and pathophysiological pathways, particularly, oncogenesis. But, the molecular pathways that govern the cell response to EGCG are not fully elucidated. The present study investigated the intracellular mechanism in oral squamous cell carcinoma (OSCC) cells treated with EGCG, focusing on HIF-1 expression and its effect on epithelial phenotype. EGCG decreased phosphorylated Raf-1 protein in YD 8 OSCC cell, but B-raf protein was not affected at all by EGCG and TF. In addition, we here found that EGCG regulated HIF-1α expression independent of Raf-1 protein. Taken together with our previous result, the result imply that EGCG is attributed to the HIF-1α expression via Raf/MEK/ERK pathway, and the HIF-1α expression is associated with the change of epithelial phenotype in OSCC cell.

Adherent cells, such as those found in epithelial tissues, must be physically associated with extracellular matrix (ECM)components to survive. Though stimulation by growth factors is an essential factor in cell survival, normal cells also requires cell adhesion to ECM proteins. The cessation of these anchorage-mediated signals seems to be a common mechanism to physiolog ically t erminate t he l ife cycle of t hese c ells b y apoptosis. This form o f cell death has been termed anoikis.In cancer, resistance to anoikis of cancer cell is important in invasion and metastasis. The present study investigated the intracellular mechanism involved in anoikis, especially in cells treated with epigallocatechin- 3-gallate(EGCG). To induce anoikis, cell culture plates were coated with 10 ㎍/ml poly-HEMA. A549 lung adenocarcinoma cells were grown in RPMI 1640 medium with/without 10% fetal bovine serum, and then cells were replated on cell culture dishes coated with poly-HEMA in the presence or absence of serum. On the other hand, EGFR inhibitor, PI3K inhibitor, and EGCG were treated to the anoikis status cells, in order to evaluate the factors of anoikis. The result revealed that growth factors or loss of adhesion can increase phosphorylate Akt. In addition, lack of cell adhesion fails to activate pro-apoptotic factors directly. Activity of Erk kinase depends on not only EGFR signaling but also cell adhesion. Akt activation is mainly affected by EGCG whereas Raf-1 activation is controlled by the presence of cell contact. In addition, EGCG increased the level of NFkB, whereas phophroylated PTEN and total PTEN were not different. In this report,increase of NFkB was correlated with Akt phosphorylation, suggesting that EGCG can protect cells from detachment–induced cell death through Akt activation and subsequent NFkB

Green tea, derived from the plant Camellia sinensis, is one of the most common beverages consumed worldwide. Epigallocatechin-3-gallate (EGCG) is the most abundant and bioactive polyphenolic constituent in green tea. Understanding how intracellular signaling pathways respond to EGCG may provide a clue to the difference of cell responses and basis for usefulness of EGCG as a chemopreventive and/or chemotherapeutic agent. In the present study, we tried to check whether EGCG could be a useful agent in chemotherapeutic treatment of oral squamous carcinoma. Furthermore, we investigated which signaling pathway is involved in biologic activities of EGCG. EGCG induced the cell death of oral squamous carcinoma cells. Furthermore, it increased phosphorylation of Akt in serum-strarved oral squamous carcinoma cells. But, initial increase of Akt activation did not affect cell survival. Activities of Raf-1 and Erk showed inconsistent response to EGCG treatment, but Erk phosphorylation is consistent with Raf-1 activity in YD 10B cells. These changes of Raf-1 and Erk activity in EGCG treated cells were different depending on cell line type. Supposedly, the difference of cell component may affect the Raf-1 and Erk reactivity to EGCG treatment. Akt activation by EGCG is independent on activities of PDK1 and PTEN, and expression of bax and bcl-2 proteins were not changed by EGCG treatment. Therefore, EGCG treatment did not induce the apoptosis of YD 10B cell. On the other hand, vascular adhesion molecule (VCAM) was decreased by EGCG treatment, so it is possible that decrease of VCAM can play certain role in survival and/or cell death in EGCG treated cells

The major component of green tea is (-)-epigallocatechin-3-gallate(EGCG) which accounts for 5080% of catechin, representing 200300 mg in a brewed cup of green tea. EGCG has been known to possess growth inhibitory and pro-apoptotic effect on human cancer cell lines such as prostate, bladder and breast cancers. In contrast, several studies have suggested that EGCG could promote cell proliferation and/or survival instead of pro-apoptotic effect. Understanding how intracellular signaling pathways respond to EGCG may provide a clue to the difference of cell responses and basis for usefulness of EGCG as a chemopreventive and/or chemotherapeutic agent. To better understand the mechanisms responsible for the chemopreventive efficacy of EGCG, the authors tried to identify the key molecules that contributes to Akt activation and can inhibit this activation. In the present study, EGCG increased Akt phosphorylation, an activeform of Akt and negatively affect on direct upstream molecules of Akt including PTEN and EGFR, though Akt phosphorylation was increased.

( - ) -epigall ocatechin - 3 -ga ll ate(EGCG) 는 녹차에서 추출되는 주된 성분으로 항산화. 세포 증식 억제 및 세 포 자멸사를 유도힌다 고 알려져 있다‘ 현 재 끼지의 여러 연구에 의하띤 EGCG는 세 포 성장을 억제하고 나아가서는 apoptoS1S까지도 유발한다. 한편 일부 연구는 EGCG가 오히려 apo ptosi s를 억 제 하고， 세 포 증식을 촉진한다고 보고하고 있다. 저자들은 EGCG가 이러한 상반된 효과틀을 보이게 되 는 기전과 그에 관련된 물질들을 파악하고지 하였다， EGCG를 세포에 처리시 초기에는 세포 생존에 관여힌다고 알려진 인 산화된 Akt 단백이 증가함이 관찰되었다 그 외에도 인산화된 Erk 단백 등의 증가로 EGCG가 세포 생존을 지속시키 는 역할을 하고 있음을 알 수 있었다‘ 이러한 현상은 COS7 과 A549 세 포 에서 관찰되었으며 Hela 세포에서는 관찰되지 않아 세 포외부에서 EGCG가 결합하게 되 는 물질 혹은 세 포내 물질 등의 차이에 의해 세 포 미다 EGCG에 대한 반응이 다른 것으로 추측된다 24시간 이상 처리된 경우 ECCG가 세 포 생존에 관린된 인자들을 감소시키는 것으로 보아 EGCG에 처음에는 세 포 생존을 유도하지만 장시간 처리 시 세 포 증식 및 생존을 억제하는 물질 임 을 확인하였다.

In t his study, we tried to identify the key elements that respond to EGCG t reatment and its role in cell survival 0 1' apop tosis by EGCG. focusing on Akt pathway and Raf-MEK-ERK pathways. Cells were serum starved for 16 h and then treated with (-) -epiga llocatechin-3-gallate. To cletermine which pathway is related to effects of EGCG on cell s, the levels of phosphorylated Akt(pAkt) and Erk (pErk) were a nalyzed by immunoblotting. A549 cell s showed the increase of pAkt in response to EGCG‘ whereas Hela cells exhi bited no difference in the levels of pAkt by EGCG treatment Phos phorylation of Akt over initial basal levels became evident a fter 1 h of EGCG treatment and peaked at 3 h pErk was also increased by EGCG in Hela cells as well as in A549 cells To determine th e effect of EGCG on growth of cells‘ A549 cells were treated wi th vari 。u s concentrations of EGCG (from 10 μ M to 300 μ M) for 3 h. Cell growth was examined by MTI assay. The resulting growth curves of A549 cell s showed that EGCG promotecl cell prolifera tion in a close-dependent manner at early phase. When cells were t rea ted with EGCG for 24 h. pAkt and pErk expressions were significantly i띠1ibited ， even at 10 μ M B-raf ex pression was also clecreased in a close-dependent manner. In teresti ngly. the presence of serum weakened t his inhibitory effect of EGCG on the ex pression of survival facto rs. Our study inrucates that EGCG stimulates cell survival of A549 cells through thc PI3K/AKT pathway. though it fina lly be haves like a suppressive agent on cell su rvival