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      • KCI등재

        소화기증상을 동반한 섬유근육통 환자에 대한 오두탕 치험 1례

        장혜연,유상구,김도형,이영수,Jang, Hye-yeon,Yu, Sang-gu,Kim, Do-hyeong,Lee, Young-su 대한한방내과학회 2021 大韓韓方內科學會誌 Vol.42 No.5

        Objective: The purpose of this study was to investigate the effects of Korean medical treatment on a fibromyalgia patient with gastrointestinal symptoms, using herbal medicines selected according to new rather than existing standards. Method: A 52-year-old female patient with fibromyalgia was treated with Odu-tang and acupuncture, cupping, and moxibustion for 22 days. To evaluate the treatment, we used the Numerical Rating Scale (NRS), American College of Rheumatology's Preliminary Diagnostic Criteria (ACR), and Korean Gastrointestinal Symptom Rating Scale (KGSRS). Result: Following treatment, pantalgia diminished, NRS, and ACR scores improved, and the GSRS score decreased from 29 to 11. Conclusion: This study suggests that Korean medical treatment could effectively reduce pain and improve digestive symptoms in patients with fibromyalgia. It also presents a new method that considers individual characteristics when choosing herbal medicine.

      • SCOPUSKCI등재

        영양분이 결핍된 H460 세포주에서 자가포식이 세포사멸에 미치는 영향

        장혜연 ( Hye Yeon Jang ),조향정 ( Hyang Jeong Jo ),황기은 ( Ki Eun Hwhang ),김소영 ( So Young Kim ),이강규 ( Kang Kyoo Lee ),문성록 ( Sun Rock Moon ),신정현 ( Jeong Hyun Shin ),조경화 ( Kyung Hwa Cho ),이미경 ( Mi Kung Lee ),이삼 대한결핵 및 호흡기학회 2010 Tuberculosis and Respiratory Diseases Vol.69 No.2

        Background: Autophagy is an important adaptive mechanism in normal development and in response to changing environmental stimuli in cancer. Previous papers have reported that different types of cancer underwent autophagy to obtain amino acids as energy source of dying cells in nutrient-deprived conditions. However, whether or not autophagy in the process of lung cancer causes death or survival is controversial. Therefore in this study, we investigated whether nutrient deprivation induces autophagy in human H460 lung cancer cells. Methods: H460, lung cancer cells were incubated in RPMI 1640 medium, and the starved media, which are BME and RPMI media without serum, including 2-deoxyl-D-glucose according to time dependence. To evaluate the viability and find out the mechanism of cell death under nutrient-deprived conditions, the MTT assay and flow cytometry were done and analyzed the apoptotic and autophagic related proteins. It is also measured the development of acidic vascular organelles by acridine orange. Results: The nutrient-deprived cancer cell is relatively sensitive to cell death rather than normal nutrition. Massive cytoplasmic vacuolization was seen under nutrient-deprived conditions. Autophagic vacuoles were visible at approximately 12 h and as time ran out, vacuoles became larger and denser with the increasing number of vacuoles. In addition, the proportion of acridine orange stain-positive cells increased according to time dependence. Localization of GFP-LC3 in cytoplasm and expression of LC-3II and Beclin 1 were increased according to time dependence on nutrient-deprived cells. Conclusion: Nutrient deprivation induces cell death through autophagy in H460 lung cancer cells.

      • KCI등재후보

        2D 나노소재기반 광 센서 소자의 최근 연구 동향

        장혜연(Hye Yeon Jang),남재현(Jae Hyeon Nam),조병진(Byungjin Cho) 한국세라믹학회 2019 세라미스트 Vol.22 No.1

        Atomically thin two-dimensional (2D) nanomaterials, including transition metal dichalcogenides (TMDs), graphene, boron nitride, and black phosphorus, have opened up new opportunities for the next generation optoelectronics owing to their unique properties such as high absorbance coefficient, high carrier mobility, tunable band gap, strong light-matter interaction, and flexibility. In this review, photodetectors based on 2D nanomaterials are classified with respect to critical element technology (e.g., active channel, contact, interface, and passivation). We discuss key ideas for improving the performance of the 2D photodetectors. In addition, figure-of-merits (responsivity, detectivity, response speed, and wavelength spectrum range) are compared to evaluate the performance of diverse 2D photodetectors. In order to achieve highly reliable 2D photodetectors, in-depth studies on material synthesis, device structure, and integration process are still essential. We hope that this review article is able to render the inspiration for the breakthrough of the 2D photodetector research field.

      • KCI등재

        Anthocyanin의 Delphinidin이 MDA-MB-231 유방암세포에 미치는 영향

        장혜연(Hye-Yeon Jang),이송희(Song-Hee Lee),안인정(In-Jung An),이해님(Hae-Nim Lee),김혜리(Hye-Ri Kim),박영석(Young-Seok Park),박병권(Byung-Kwon Park),김병수(Byeong-Soo Kim),김상기(Sang-Ki Kim),조성대(Sung-Dae Cho),남정석(Jeong-Seok Na 한국식품영양과학회 2014 한국식품영양과학회지 Vol.43 No.2

        본 연구에서는 블루베리에 포함된 anthocyanin 중 delphinidin이 인간 유래의 MDA-MB-231 유방암세포의 성장을 억제시키고 apoptosis를 유발하는지 살펴보고 in vivo 실험에서도 항암효과가 나타나는지 확인하였다. 그 결과 cell viability를 보기 위한 MTT assay에서는 농도 의존적으로암세포의 성장을 억제시켰으며, apoptosis의 확인을 위한 DAPI stain에서 농도 의존적으로 chromatin condensation이 유의적으로 증가하는 것을 확인하였다. 또한 western blot에서 암 억제 유전자인 p53 단백질이 증가하였고, anti-apoptotic 분자인 Bcl-2 단백질과 p-GSK3β 단백질은 감소하였다. In vivo 실험에서는 대조군과 비교해 10 mg/kg delphinidin을 투여한 군에서 종양의 크기가 감소하였으며, TUNEL assay를 통해 apoptosis 세포 또한 통계학적으로 유의적인 증가가 관찰되어 종양 억제 효과를 확인하였다. 이상의 결과들로 볼 때, MDA-MB-231 유방암세포에서 delphinidin은 암세포의 증식을 억제시키고, apoptosis를 유발시키는 효과를 보이므로 암 예방제나 치료제로 개발될 수 있을 것으로 사료된다. This research showed that delphinidin, an anthocyanin present in blueberry, induced apoptosis in MDA-MB-231 breast cancer cells as well as mediated anti-cancer effects in vivo. As a result, growth of cancer cells as assessed by MTT assay decreased in a concentration-dependent manner. Chromatin condensation by DAPI staining significantly increased in a concentration-dependent manner, indicating apoptosis. The level of p53-protein increased while those of anti-apoptotic molecules (Bcl-2, p-GSK3β) decreased in the western blot. Tumor size decreased in cells treated with 10 mg/kg of delphinidin compared with the control group in vivo. Cell apoptosis assessed by TUNEL assay significantly increased, and tumor inhibitory effect was confirmed. Therefore, delphinidin can be developed for cancer preventive medicine due to its growth inhibitory effects and induction of apoptosis in human breast cancer cells.

      • KCI등재

        신생 매일지속두통 환자에 대한 통합 한방치료 증례보고

        유상구,장혜연,김민주,박철우,이세원,전상우,Yu, Sang-gu,Jang, Hye-yeon,Kim, Min-ju,Park, Cheol-u,Lee, Se-won,Jeon, Sang-woo 대한한방내과학회 2021 大韓韓方內科學會誌 Vol.42 No.2

        Objectives: This case report presents the effects of Korean medicine treatment in a patient with a new daily, persistent headache. Methods: A 58-year-old female patient with a new daily, persistent headache was treated with Yonggakgyodaeyeong-tang and Kyoungbang Chungsanggyuntong-tang granules, acupuncture, pharmacopuncture, and chuna therapy for 68 days. Headache and neck disability were assessed using a numeric rating scale (NRS), the headache impact test-6 (HIT-6), and the neck disability index (NDI). Results: After 68 days of treatment, headache was relieved, as measured by an NRS decrease from 7 to 4. In addition, the HIT score decreased from 30 to 18, and the NDI score decreased from 42 to 20. Conclusion: These results show that a daily, persistent headache can be relieved with Korean medicine treatment. However, additional well-designed studies are required to confirm these findings.

      • SCOPUSKCI등재

        폐암세포주에서 저용량 시스플라틴에 의해 유도된 자가포식

        신정현 ( Jeong Hyun Shin ),장혜연 ( Hye Yeon Jang ),정진수 ( Jin Soo Chung ),조경화 ( Kyung Hwa Cho ),황기은 ( Ki Eun Hwang ),김소영 ( So Young Kim ),김휘정 ( Hui Jung Kim ),이삼윤 ( Sam Youn Lee ),이미경 ( Mi Kung Lee ),박순아 ( 대한결핵 및 호흡기학회 2010 Tuberculosis and Respiratory Diseases Vol.69 No.1

        Background: Most lung cancer patients receive systemic chemotherapy at an advanced stage disease. Cisplatin-based chemotherapy is the main regimen for treating advanced lung cancer. Recently, autophagy has become an important mechanism of cellular adaptation under starvation or cell oxidative stress. The purpose of this study was to determine whether or not autophagy can occurred in cisplatin-treated lung cancer cells. Methods: H460 cells were incubated with RPMI 1640 and treated in 5 μM or 20 μM cisplatin concentrations at specific time intervals. Cells surviving cisplatin treatment were measured and compared using an MTT cell viability assay to cells that underwent apoptosis with autophagy by nuclear staining, apoptotic or autophagic related proteins, and autophagic vacuoles. The development of acidic vascular organelles was using acridine orange staining and fluorescent expression of GFP-LC3 protein in its transfected cells was observed to evaluate autophagy. Results: Lung cancer cells treated with 5 μM cisplatin-treated were less sensitive to cell death than 20 μM cisplatin-treated cells in a time-dependent manner. Nuclear fragmentation at 5 μM was not detected, even though it was discovered at 20 μM. Poly (ADP-ribose) polymerase cleavages were not detected in 5 μM within 24 hours. Massive vacuolization in the cytoplasm of 5 μM treated cells were observed. Acridine orange stain-positive cells was increased according in time-dependence manner. The autophagosome-incorporated LC3 II protein expression was increased in 5 μM treated cells, but was not detected in 20 μM treated cells. The expression of GFP-LC3 were increased in 5 μM treated cells in a time-dependent manner. Conclusion: The induction of autophagy occurred in 5 μM dose of cisplatin-treated lung cancer cells.

      • KCI등재
      • KCI등재

        피세아타놀에 의한 YD-15 구강암세포의 세포자가사멸 유도 효과

        이해님(Hae-Nim Lee),장혜연(Hye-Yeon Jang),김형진(Hyeong-Jin Kim),신성아(Seong-Ah Shin),추강식(Gang-Sik Choo),박병권(Byung-Kwon Park),김병수(Byeong-Soo Kim),정지윤(Ji-Youn Jung) 한국식품영양과학회 2015 한국식품영양과학회지 Vol.44 No.7

        Resveratrol 유도체의 일종으로 stilbene 계열 물질인 piceatannol은 암세포의 증식을 억제하고 apoptosis를 유발하는 것으로 알려져 있다. 본 연구에서는 YD-15 인체 구강암세포를 대상으로 piceatannol에 의한 암세포 증식 억제와 연관된 부가적인 기전연구를 실시하였다. Piceatannol이 암세포 성장에 미치는 영향을 확인하기 위하여 구강암세포주 YD-15에 piceatannol을 0, 6.25, 12.5, 25, 50, 100, 200 μM의 농도로 처리하고 MTT assay를 수행한 결과 piceatannol은 농도 의존적으로 세포 성장을 억제하였다. Piceatannol에 의한 암세포 증식 억제 효과가 apoptosis에 의한 것인지 확인하기 위해 DAPI 염색을 수행한 결과 apoptotic body와 세포질 응축이 농도 의존적으로 증가하는 것을 확인하였다. Western blotting의 결과 piceatannol은 Bax와 cleaved-PARP 단백질의 발현을 농도 의존적으로 증가시키고 Bcl-2 단백질 발현을 감소시켰다. In vivo 실험에서는 누드마우스에 YD-15 구강암세포를 이종이식한 후 3주간의 piceatannol 복강투여를 통해 이식된 종양의 크기를 측정한 결과 piceatannol 처치군이 대조군에 비해 유의적으로 종양부피가 감소하였고, 종양조직을 이용해 TUNEL assay를 수행한 결과 piceatannol 처치군에서 TUNEL-positive cell이 더 많이 관찰되었다. 또한 종양조직을 이용해 IHC stain을 수행하여 cleaved-caspase-3와 Ki-67을 확인한 결과 piceatannol 처치군에서 cleaved-caspase-3가 증가하는 경향을 보였고 Ki-67은 감소하는 경향을 보였다. 따라서 piceatannol은 인체 구강암세포에서 apoptosis를 유도시키고 종양 형성을 억제함으로써 구강암 치료제로의 개발 가능성이 있는 것으로 확인하였다. Piceatannol (trans-3,4,3",5"-trihydroxystilbene), a natural stilbene, is an analogue of resveratrol. In the present study, possible mechanisms by which piceatannol exerts its pro-apoptotic action in cultured human oral cancer YD-15 cells were investigated. To investigate whether or not piceatannol has effects on cancer cell viability, human oral YD-15 cells were treated with piceatannol (0, 50, and 100 μM). Piceatannol treatment (100 μM) showed the strongest inhibition of cell proliferation and reduced cell viability in a dose-dependent manner. Chromatin condensation detected by DAPI staining significantly increased in a concentration-dependent manner, indicating apoptosis. Piceatannol treatment activated initiator Bax (pro-apoptotic) and cPARP in a concentration-dependent manner. Further, piceatannol induced down-regulation of Bcl-2 (anti-apoptotic). We also evaluated the activity of piceatannol against oral cavity cancer tumors in mice. Piceatannol-treated nude mice bearing YD-15 xenograft tumors exhibited significantly reduced tumor volume and weight due to the potent effect of piceatannol on tumor cell apoptosis, as determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay. Immunohistochemistry staining showed elevated expression of cleaved-caspase-3 as well as reduced expression of Ki-67 in the piceatannol-treated group. Therefore, piceatannol can be developed as a cancer preventive medicine due to its growth inhibitory effects and induction of apoptosis in human oral cancer cells.

      • SCOPUSKCI등재

        폐암세포주에서 Heme Oxygenase-1의 억제가 Cisplatin의 항암제 감수성에 미치는 영향

        김소영 ( So Young Kim ),김은정 ( Eun Jung Kim ),장혜연 ( Hye Yeon Jang ),황기은 ( Ki Eun Hwang ),박정현 ( Jung Hyun Park ),김휘정 ( Hwi Jung Kim ),조향정 ( Hyang Jeong Jo ),양세훈 ( Sei Hoon Yang ),정은택 ( Eun Taik Jeong ),김학렬 대한결핵 및 호흡기학회 2007 Tuberculosis and Respiratory Diseases Vol.62 No.1

        연구배경: 다양한 고형암에서 HO-1의 높은 발현이 알려져 있고, 그것의 항산화와 항세포고사의 역할로 인해 빠른 암종의 성장에 중요한 역할이 있음이 보고되고 있다. 대표적인 활성산소종 생성 항암제인 Cisplatin은 현재까지 폐암치료에 가장 광범위하게 사용되고 있으나, 여러 내성발생이 임상치료의 주요문제로 대두되고 있다. 저자들은 A549 폐암세포주에서 HO-1의 발현이 증가되었고 HO-1 활성억제제나 siRNA 방법을 통해 생존율의 의미 있는 감소와 세포고사가 유도됨을 보고한 바 있다. 이 연구의 목적은 A549 폐암세포주에 cisplatin 처리시 HO-1의 발현의 증가유무와 기전을 규명하고 실제 HO-1의 억제가 cisplatin에 의한 항암제 감수성을 증가시키는지를 알아보는데 있다. 방법: 비소세포폐암세포주인 A549, NCI-H23, NCI-H157, NCI-H460을 이용하였다. 세포독성은 MTT 방법으로 구하였고, HO-1, Nrf2, MAPK의 발현은 Western blotting으로 확인하였다. 또한 MAPK억제제들을 전처치한 후 cisplatin에 의해 유도된 Nrf2와 HO-1의 발현에 미치는 영향을 역시 Western blotting으로 관찰하였다. A549세포에 활성억제제인 ZnPP나 HO-1 small interfering RNA (siRNA)을 주입하여 cisplatin과의 병합요법시 생존율의 배가효과 유무를 MTT 방법으로 확인하였고, 이러한 효과가 ROS 형성과 HO-1의 발현변화와 관련되는지를 알아보기 위해 carboxy-H2DCFDA 방법과 Western blotting을 통해 각각 확인하였다. 결과: Cisplatin 처리시 다른 세포주에 비해 A549세포가 의의 있게 내성을 보였다. 10μM의 농도에서 시간 의존적으로 HO-1, Nrf2, MAPK의 발현이 증가하였고, MAPK 억제제들을 전 처치하였을 때 cisplatin에 의해 유도된 HO-1과 Nrf2의 발현이 억제됨을 확인하였다. HO-1의 활성억제제인 ZnPP와 HO-1 siRNA를 통해 HO-1 mRNA를 직접 억제하는 방법으로 cisplatin과 병합치료시 단독치료에 비해 의의 있는 생존율의 감소를 보였다. 이러한 효과는 활성산소종의 생성 증가와 HO-1의 발현억제에 의한 결과임을 확인하였다. 결론: Cisplatin 처리시 HO-1의 발현은 MAPK-Nrf2-HO-1의 경로를 통해 증가하였고, 부분적으로 치료에 대한 내성과 관련이 있었으며, ZnPP 등의 활성억제제나 siRNA를 통한 knock-down 방법으로 HO-1을 표적으로 억제하는 치료방법을 통해 cisplatin의 항암제 감수성을 증가시켰다. Background: Heme oxygenase-1 (HO-1) is known to modulates the cellular functions, including cell proliferation and apoptosis. It is known that a high level of HO-1 expression is found in many tumors, and HO-1 plays an important role in rapid tumor growth on account of its antioxidant and antiapoptotic effects. Cisplatin is a widely used anti-cancer agent for the treatment of lung cancer. However, the development of resistance to cisplatin is a major obstacle to its use in clinical treatment. We previously demonstrated that inhibiting HO-1 expression through the transcriptional activation of Nrf2 induces apoptosis in A549 cells. The aim of this study was to determine of the inhibiting HO-1 enhance the chemosensitivity of A549 cells to cisplatin. Materials and Methods: The human lung cancer cell line, A549, was treated cisplatin, and the cell viability was measured by a MTT assay. The change in HO-1, Nrf2, and MAPK expression after the cisplatin treatment was examined by Western blotting. HO-1 inhibition was suppressed by ZnPP, which is a specific pharmacologic inhibitor of HO activity, and small interfering RNA (siRNA). Flow cytometry analysis and Western blot were performed in to determine the level of apoptosis. The level of hydrogen peroxide (H2O2) generation was monitored fluoimetrically using 2`,7`-dichlorofluorescein diacetate. Results: The A549 cells showed more resistance to the cisplatin treatment than the other cell lines examined, whereas cisplatin increased the expression of HO-1 and Nrf2, as well as the phosphorylation of MAPK in a time-dependent fashion. Inhibitors of the MAPK pathway blocked the induction of HO-1 and Nrf2 by the cisplatin treatment in A549 cells. In addition, the cisplatin-treated A549 cells transfected with dither the HO-1 small interfering RNA (siRNA) or ZnPP, specific HO-1 inhibitor, showed in a more significantly decrease in viability than the cisplatin-only-treated group. The combination treatment of ZnPP and cisplatin caused in a marked increase in the ROS generation and a decrease in the HO-1 expression. Conclusion: Cisplatin increases the expression of HO-1, probably through the MAPK-Nrf2 pathway, and the inhibition of HO-1 enhances the chemosensitivity of A549 cells to cisplatin. (Tuberc Respir Dis 2007; 62: 33-42)

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