• Applied Biological Chemistry
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• 제46권1호
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• pp.50-54
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• 2003

호장근에서 분리한 emodin은 VEGF로 유도된 혈관신생의 한 단계인 혈관내피세포의 이동을 강하게 억제하였다. 또한 emodin은 혈관내피세포 이동을 억제시킨 $0.1\;{\mu}g/ml$ 농도에서 시험관내 혈관신생을 억제하였으며, 그 효과는 농도의존적인 양상을 보였다. 생체내 혈관신생 모델인 CAM assay에서도 emodin은 혈관신생을 억제하였다. 이러한 결과는 emodin이 현재까지 보고된 여러 가지 생리활성 이외에 혈관신생 억제활성을 가지고 있다는 사실을 보여주는 것이다. 따라서 emodin을 함유하고 있는 호장근은 혈관신생 관련 질환에 대한 천연물 유래 치료제의 개발을 위한 중요한 식물자원으로 활용될 수 있을 것이다.

• Biomolecules & Therapeutics
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• 제15권3호
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• pp.192-198
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• 2007

Emodin (1,3,8-trihydroxy-6-methylanthraquinone) is a major constituent of rhubarb. Although it has been claimed to have a wild spectrum of therapeutic value, its side effects, especially in human kidney cells have not been well characterized. In this study, we have carried out in vitro genetic toxicity test of emodin and microarray analysis of differentially expressed genes in response to emodin. The result of Ames test showed mutations with emodin treatment in base substitution strain TA1535 both with and without exogenous metabolic activation. Likewise, emodin showed mutations in frame shift TA98 both with and without exogenous metabolic activation. The result of COMET assay in L5178Y cells with emodin treatment showed DNA damage both with and without exogenous metabolic activation. Emodin did not increase micronuclei in CHO cells both with and without exogenous metabolic activation. 150 Genes were selected as differentially expressed genes in response to emodin by microarray analysis and these genes would be candidate biomarkers of genetic toxic action of emodin.

• 생명과학회지
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• 제31권10호
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• pp.929-936
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• 2021

본 연구에서는 시판하는 천연물 library (Selleckchem, L1400)로부터 암세포 항 성장 활성을 보여주는 천연물을 선별하였다. 즉, 인간 대장암 세포주인 HCT116에 50 μM의 각 천연물을 처리한 후 세포 생존율을 측정하였다. 1차 선별과정을 통하여 5종의 천연물(chrysin, diosmetin, emodin, piperlongumine, tanshinone I)을 선별하였다. 5종의 천연물에 의한 NAG-1 단백질의 발현을 확인한 결과 chrysin과 emodin에 의해서 발현이 현저하게 증가하였다. 또한, chrysin과 emodin은 농도의존적으로 세포 생존율을 감소시켰으며, chrysin과 emodin은 항암 단백질인 NAG-1의 발현을 농도 및 시간 의존적으로 증가시켰다. 게다가, chrysin과 emodin 처리에 의해 증가된 PARP cleavage가 NAG-1 siRNA transfection에 의해서 감소됨을 확인함으로써, chrysin과 emodin에 의한 세포사멸과 NAG-1의 발현 증가가 직접적인 관련이 있음을 증명하였다. 따라서, 본 연구결과는 암세포 항 성장 활성을 보여주는 천연물 선별에 대한 기초 데이터를 제공해 주며, chrysin과 emodin에 의한 암세포 항 성장 활성 및 세포사멸의 기전을 이해하는 데 도움을 줄 것으로 판단된다.

• Biomolecules & Therapeutics
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• 제24권4호
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• pp.395-401
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• 2016

Endochondral bone formation is the process by which mesenchymal cells condense into chondrocytes, which are ultimately responsible for new bone formation. The processes of chondrogenic differentiation and hypertrophy are critical for bone formation and are therefore highly regulated. The present study was designed to investigate the effect of aloe-emodin on chondrogenic differentiation in clonal mouse chondrogenic ATDC5 cells. Aloe-emodin treatment stimulated the accumulation of cartilage nodules in a dose-dependent manner. ATDC5 cells were treated with aloe-emodin and stained with alcian blue. Compared with the control cells, the ATDC5 cells showed more intense alcian blue staining. This finding suggested that aloe-emodin induced the synthesis of matrix proteoglycans and increased the activity of alkaline phosphatase. Aloe-emodin also enhanced the expressions of chondrogenic marker genes such as collagen II, collagen X, BSP and RunX2 in a time-dependent manner. Furthermore, examination of the MAPK signaling pathway showed that aloe-emodin increased the activation of extracellular signal-regulated kinase (ERK), but had no effect on p38 and c-jun N-terminal kinase (JNK). Aloe-emodin also enhanced the protein expression of BMP-2 in a time-dependent manner. Thus, these results showed that aloe-emodin exhibited chodromodulating effects via the BMP-2 or ERK signaling pathway. Aloe-emodin may have potential future applications for the treatment of growth disorders.

• 한국한의학연구원논문집
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• 제13권1호통권19호
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• pp.139-145
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• 2007

Emodin is one of the main active components of a traditional Korean medicine isolated from the root and rhizomes of Rheum palmatum L. In this study, of 222 natural compounds to evaluate the anabolic activities, emodin activated bone morphogenetic protein (BMP)-2 promoter in the differentiation process of mouse osteoblastic MC3T3-E1 cells. Emodin was shown to significantly stimulate the activity and expression of alkaline phosphatase, an earlyphase marker of osteoblastic differentiation, on the differentiation day 7, and induce the osteopontin mRNA expression from the differentiation day 14. In addition, low concentration (up to 5 M) of emodin dramatically promoted the induction of mineralization in MC3T3-E1 subclone 4 cells. The stimulatory effect of emodin on the osteoblast differentiation/mineralization could be associated with its potential to stimulate the BMP-2 gene expression. Although further studies are needed to determine the precise mechanism, this study suggests that the use of herbal medicine containing natural compounds with anabolic activity such as emodin could have a beneficial effect on bone health.

• Applied Biological Chemistry
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• 제27권3호
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• pp.151-157
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• 1984

Penicillium islandicum은 Czapek-Dox 배지를 이용하여 어두운 곳에서 배양되었을때 황적색 색소인 skyrin을 생합성 하였다. $[^{14}C]$-acetate 배지에 이 균주를 접종 배양하여 얻어진 대사산물로부터 radioactive skyrin을 순수 정제 분리할 수 있었고 이를 sodium dithionite 처리하여 Emodin이 합성되는 것을 동정할 수 있었다. 한편, Penicillium islandicum의 배양액에서 추출 정제된 효소를 이용한 균체의 효소실험에서 $[^3H]$-emodin과 $[^3H]$-emodin은 skyrin생합성의 유력한 전구체물질임이 밝혀졌으며, 효소반응결과 $[^3H]$ emodinanthrone(4.8%)이 $[^3H]$-emodin보다 radioactive skyrin으로 주입되는 비율이 더 크다는 것을 알 수 있었다. 균체외 효소실험결과, skyrin이 생합성되는 경로는 $emodinanthrone{\rightarrow}emodin{\rightarrow}skyrin$으로 진행되었다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권13호
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• pp.5201-5205
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• 2014

Emodin, a natural anthraquinone isolated from the traditional Chinese medicine Radix rhizoma Rhei, can induce apoptosis in many kinds of cancer cells. This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway. Emodin induced mitochondrial transmembrane potential loss, increase in Bax and decrease in Bcl-2 expression and mitochondrial translocation and release of cytochrome c to cytosol in HCT116 cells. In response to emodin-treatment, ROS increased rapidly, and subsequently p53 was overexpressed. Pretreatment with the antioxidant NAC diminished apoptosis and p53 overexpression induced by emodin. Transfecting p53 siRNA also attenuated apoptosis induced by emodin, Bax expression and mitochondrial translocation being reduced compared to treatment with emodin alone. Taken together, these results indicate that ROS is a trigger of emodin-induced apoptosis in HCT116 cells, and p53 expression increases under oxidative stress, leading to Bax-mediated mitochondrial apoptosis.

• Journal of Nutrition and Health
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• 제52권2호
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• pp.176-184
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• 2019

Purpose: Protein overloading in the endoplasmic reticulum (ER) leads to endoplasmic reticulum stress, which exacerbates various disease conditions. Emodin, an anthraquinone compound, is known to have several health benefits. The effect of emodin against palmitic acid (PA) - induced ER stress in HepG2 cells was investigated. Methods: HepG2 cells were treated with varying concentrations of palmitic acid to determine the working concentration that induced ER stress. ER stress associated genes such as ATF4, XBP1s, CHOP and GRP78 were checked using RT- PCR. In addition, the expression levels of unfolded protein response (UPR) associated proteins such as $IRE1{\alpha}$, $eIF2{\alpha}$ and CHOP were checked using immunoblotting to confirm the induction of ER stress. The effect of emodin on ER stress was analyzed by treating HepG2 cells with $750{\mu}M$ palmitic acid and varying concentrations of emodin, then analyzing the expression of UPR associated genes. Results: It was evident from the mRNA and protein expression results that palmitic acid significantly increased the expression of UPR associated genes and thereby induced ER stress. Subsequent treatment with emodin reduced the mRNA expression of ATF4, GRP78, and XBP1s. Furthermore, the protein levels of $p-IRE1{\alpha}$, $p-eIF2{\alpha}$ and CHOP were also reduced by the treatment of emodin. Analysis of sirtuin mRNA expression showed that emodin increased the levels of SIRT4 and SIRT7, indicating a possible role in decreasing the expression of UPR-related genes. Conclusion: Altogether, the results suggest that emodin could exert a protective effect against fatty acid-induced ER stress and could be an agent for the management of various ER stress related diseases.

• 동의생리병리학회지
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• 제25권6호
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• pp.1039-1043
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• 2011

The purpose of this study is to investigate the modulatory effect of emodin on hydrogen peroxide production in human blastoma SH-SY5Y cells induced by the synthetic analog of double-stranded RNA [polyinosinic-polycytidylic acid]. Hydrogen peroxide production was measured by dihydrorhodamine 123 (DHR) assay. Emodin significantly inhibited the polyinosinic-polycytidylic acid (PIC)-induced production of hydrogen peroxide for 0.5, 2, 12, 18, and 24 hr incubation at the concentrations of 5, 10, 25, and 50 uM in SH-SY5Y (P < 0.05) in dose dependent manner. These results suggest that emodin has neuroprotective property related with its inhibition of hydrogen peroxide production in PIC-induced neuronal cells.

• 약학회지
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• 제54권5호
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• pp.387-391
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• 2010

Polygonum cuspidatum which is widely distributed in Korea has been used as treatments of dermatitis, gonorrhea and inflammation in traditional medicine. We examined anti-inflammatory activities by the inhibition of NO production in RAW264.7 murine macrophages cells. Phytochemical examination of Polygonum cuspidatum led to the isolation and characterization of emodin (1), emodin 8-O-${\beta}$-D-glucopyranoside (2), emodin 1-O-${\beta}$-D-glucopyranoside (3). Antioxidative activities of these compounds were determined by measuring the radical scavenging effects on DPPH radicals. Compounds 1 and 3 showed potent activities compared with L-NMMA. These results suggested that the antraquinone compounds isolated from Polygonum cuspidatum might be used as antiinflammatory agents.