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Park, Euteum,Chun, Hong Sung Wolters Kluwer Health | Lippincott Williams Wilkin 2016 NEUROREPORT - Vol.27 No.15
<P>Dieldrin, an organochlorine pesticide still used in several developing countries, has been proposed as a risk factor for Parkinson's disease. Quercetin is one of the potent bioactive flavonoids present in numerous plants. In this study, we investigated the protective effects of quercetin on neurotoxicity induced by dieldrin in cultured dopaminergic SN4741 cells. Our initial experiments showed that quercetin (10-40M) dose dependently prevented dieldrin (20M)-induced cytotoxicity in SN4741 cells. Pretreatment for 1h with quercetin before dieldrin application could significantly suppress dieldrin-induced apoptotic characteristics, including nuclear condensation, DNA fragmentation, and caspase-3/7 activation. Results showed that dieldrin-induced markers of endoplasmic reticulum (ER) stress response such as chaperone GRP78, heme oxygenase-1, and phosphorylation of the subunit of eukaryotic initiation factor 2. In addition, dieldrin reduced antiapoptotic Bcl-2 expression, but significantly elevated a proapoptotic transcription factor CHOP. Furthermore, RNA interference to CHOP almost completely repressed dieldrin-induced apoptotic cell death. Interestingly, quercetin prevented the changes in dieldrin-induced ER stress markers. These results suggest that quercetin may suppress the ER stress-CHOP pathway and dieldrin-induced apoptosis in dopaminergic neurons.</P>
Resveratrol Inhibits Lipopolysaccharide-induced Phagocytotic Activity in BV2 cells
Park, Euteum,Kim, Do Kyung,Chun, Hong Sung 한국응용생명화학회 2012 Applied Biological Chemistry (Appl Biol Chem) Vol.55 No.6
The inhibitory effects of resveratrol, a natural bioactive polyphenolic phytoalexin rich in grape, on lipopolysaccharide (LPS)-induced microglial activation and its beneficial effects on dopaminergic neurodegeneration were studied. Resveratrol dose-dependently suppressed LPS-induced nitric oxide production and the expression of inducible NO synthase (iNOS) in BV-2 microglial cells. Furthermore, resveratrol ($1{\mu}M$) significantly blocked BV2 microglial phagocytosis induced by LPS ($0.1{\mu}g/mL$). Although the conditioned media from LPS-stimulated BV2 cells caused the SN4741 dopaminergic neuronal cell death, that from resveratrol-pretreated BV2 cells did not diminish the viability of SN4741 cells. These results suggest that resveratrol can prevent neuronal death possibly through the modulation of phagocytosis and microglial activation.
BV-2 미세아교세포의 활성에 대한 녹차 유래 폴리페놀 EGCG의 억제 효과
박으뜸(Euteum Park),전홍성(Hong Sung Chun) 한국생명과학회 2016 생명과학회지 Vol.26 No.6
본 연구에서는 녹차 유래 polyphenol 중의 하나인 epigallocatechine gallate (EGCG)를 이용한 신경염증 억제효과를 확인하였다. LPS로 유도된 미세아교세포의 활성화로 분비되는 nitric oxide (NO)와 pro-inflammatory cytokine을 포함하여 iNOS, TNF-a와 IL-1b 유전자의 발현과 LPS 수용체인 TLR-4의 활성에 미치는 EGCG의 억제 효능을 확인하였다. Latex beads를 이용한 phagocytotic activity를 확인한 결과 LPS로 유도된 미세아교세포 활성에 의한 식균활성이 EGCG에 의해 억제되는 것을 볼 수 있었다. 뿐만 아니라, BV-2 미세아교세포 조건배지를 이용하여 도파민성 신경세포 SN4741의 세포 사멸확인에서도 EGCG에 의한 보호 효과를 확인하였다. 본 연구 결과는 녹차유래 polyphenol인 EGCG의 신경염증 반응억제효능과 신경퇴행성 질환 제어 가능성을 확인하였다. 본 연구의 결과는 녹차 유래 polyphenol인 EGCG의 신경염증 반응과 그로 인한 신경 퇴행성 질환 제어 가능성을 제시하였다. Microglial cells are immediately activated in the central nervous system in response to a variety of neuronal environmental changes, such as injuries or inflammation. In addition to the modulation of the intrinsic immune response, a key role of microglial cells is the phagocytosis of dying cells and cellular debris. In this study, the inhibitory effects of epigallocatechine-3-gallate (EGCG), a most abundant and active polyphenol component of green tea, on lipopolysaccharide (LPS)-induced microglial activation are determined. EGCG dose dependently suppressed LPS-induced nitric oxide production and the expression of inducible nitric oxide synthase (iNOS) in BV-2 microglial cells. EGCG are potent LPS-induced inhibitors of several pro-inflammatory cytokine expressions, such as TNF-α and IL-1β, in microglial cells. Furthermore, EGCG generally inhibits the induction of LPS-mediated microglial activation and potently inhibits the phagocytosis of LPS-stimulated BV2 microglia. Although the conditioned media from LPS-stimulated BV-2 cells caused the SN4741 cell death, that from the conditioned media of EGCG pretreated BV-2 cells did not diminish the viability of SN4741 cells. These results suggest EGCG, a green tea polyphenol, could be a promising available molecule for the modulation of harmful microglial activation.
MicroRNA Analysis in Normal Human Oral Keratinocytes and YD-38 Human Oral Cancer Cells
Hye Ryun Kim,Euteum Park,Kwang-Hee Cho,Do Kyung Kim KOREAN ACADAMY OF ORAL BIOLOGY 2011 International Journal of Oral Biology Vol.36 No.4
MicroRNAs (miRNAs) are small non-coding RNAs that mediate gene expression at the post-transcriptional level by degrading or repressing targeted mRNAs. These molecules are about 21-25 nucleotides in length and exert their effects by binding to partially complementary sites in mRNAs, predominantly in the 3’-untranslated region (3’-UTR). Recent evidence has demonstrated that miRNAs can function as oncogenes or tumor suppressors through the modulation of multiple oncogenic cellular processes in cancer development, including initiation, cell proliferation, apoptosis, invasion and metastasis. In our present study, we examined the expression profile of miRNAs related to oral cancer cell growth inhibition using normal human oral keratinocytes (NHOK) and YD-38 human oral cancer cells. By miRNA microassay analysis, 40 and 31 miRNAs among the 1,769 examined were found to be up- and down-regulated in YD-38 cells compared with NHOK cells, respectively. Using qRTPCR analysis, the expression levels of miR-30a and miR-1246 were found to be increased in YD-38 cells compared with NHOK cells, whereas miR-203 and miR-125a were observed to be decreased. Importantly, the overexpression of miR-203 and miR-125a significantly inhibited the growth of YD-38 cells. This finding and the microarray data indicate the involvement of specific miRNAs in the development and progression of oral cancer.
Nargenicin attenuates lipopolysaccharide-induced inflammatory responses in BV-2 cells
Yoo, Jin Cheol,Cho, Hong-Suk,Park, Euteum,Park, Jeong Ae,Kim, Seung,Kim, Do Kyung,Kim, Chun Sung,Kim, Sung-Jun,Chun, Hong Sung Lippincott Williams Wilkins, Inc. 2009 NEUROREPORT - Vol.20 No.11
Microglia activation has been considered as a major factor associated with neurodegenerative diseases. In this study, we investigated the inhibitory effects of nargenicin, a natural antibiotic from soil bacterium Nocardia, on lipopolysaccharide (LPS)-induced inflammatory activation of microglia. Nargenicin significantly attenuated LPS-induced nitric oxide production in BV-2 microglial cells. Furthermore, nargenicin effectively suppressed the upregulation of interleukin-1&bgr;, tumor necrosis factor α, and inducible nitric oxide synthase at both mRNA and protein levels in LPS-stimulated BV-2 microglia. In addition, nargenicin blocked LPS-induced degradation of I&kgr;B-α, indicating that the initial molecular target of nargenicin is the transcription factor nuclear factor-&kgr;B. These results suggest that nargenicin should be evaluated as a therapeutic agent for inflammatory neurodegenerative diseases.
정재윤(Jae-Yun Jung),박으뜸(Euteum Park),이기일(Ki-Il Lee) 대한두경부종양학회 2006 대한두경부 종양학회지 Vol.22 No.2
Trichilemmal carcinoma is a rare malignant neoplasm of the hair follicle from the outer root of the hair follicle sheath. This tumor can be misleading, and a false diagnosis of a squamous cell carcinoma. We report a case of trichilemmal carcinoma with a review of literature. The patient presented with an exophytic well circumscribed nodular mass on the left auricle, which was detected 6 months ago. Histopathologically, the tumor consisted of atypical clear cells which contained abundant glycogen. The tumor cells shows lobular growth pattern with necrosis, foci of trichilemmal keratinization and peripheral pallisading. Total excision and repair with full-thickness skin graft was done with minimal surgical morbidity. The patient has been free of recurrence or metastasis for 8 months.