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US20070155829A1 - Agent for controlling bcl-2 expression comprising ginsenoside f1 as an active component - Google Patents

Agent for controlling bcl-2 expression comprising ginsenoside f1 as an active component Download PDF

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Publication number
US20070155829A1
US20070155829A1 US10/539,012 US53901203A US2007155829A1 US 20070155829 A1 US20070155829 A1 US 20070155829A1 US 53901203 A US53901203 A US 53901203A US 2007155829 A1 US2007155829 A1 US 2007155829A1
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Prior art keywords
ginsenoside
bcl
expression
cells
treated
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US10/539,012
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English (en)
Inventor
Si-Young Cho
Eun-Hee Lee
Su-Jung Kim
Eui-Seok Shin
Hui-Kyoung Chang
Duck-Hee Kim
Myeong-Hoon Yeom
Kwang-Sik Woe
Tae-Ryong Lee
Young-Chul Sim
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Amorepacific Corp
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Amorepacific Corp
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Assigned to AMOREPACIFIC CORPORATION reassignment AMOREPACIFIC CORPORATION ASSIGNMENT OF ASSIGNORS INTEREST (SEE DOCUMENT FOR DETAILS). Assignors: LEE, EUN-HEE, SIM, YOUNG-CHUL, WOE, KWANG-SIK, CHANG, HUI-KYOUNG, CHO, SI-YOUNG, KIM, DUCK-HEE, KIM, SU-JUNG, LEE, TAE-RYONG, SHIN, EUI-SEOK, YEOM, MYENG-HOON
Publication of US20070155829A1 publication Critical patent/US20070155829A1/en
Priority to US12/135,663 priority Critical patent/US8258272B2/en
Abandoned legal-status Critical Current

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    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
    • A61K31/00—Medicinal preparations containing organic active ingredients
    • A61K31/70—Carbohydrates; Sugars; Derivatives thereof
    • A61K31/7028—Compounds having saccharide radicals attached to non-saccharide compounds by glycosidic linkages
    • A61K31/7034—Compounds having saccharide radicals attached to non-saccharide compounds by glycosidic linkages attached to a carbocyclic compound, e.g. phloridzin
    • A61K31/704—Compounds having saccharide radicals attached to non-saccharide compounds by glycosidic linkages attached to a carbocyclic compound, e.g. phloridzin attached to a condensed carbocyclic ring system, e.g. sennosides, thiocolchicosides, escin, daunorubicin
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
    • A61K31/00—Medicinal preparations containing organic active ingredients
    • A61K31/70—Carbohydrates; Sugars; Derivatives thereof
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P17/00—Drugs for dermatological disorders
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P17/00—Drugs for dermatological disorders
    • A61P17/16—Emollients or protectives, e.g. against radiation
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P35/00—Antineoplastic agents
    • A61P35/04—Antineoplastic agents specific for metastasis
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P39/00—General protective or antinoxious agents
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61P—SPECIFIC THERAPEUTIC ACTIVITY OF CHEMICAL COMPOUNDS OR MEDICINAL PREPARATIONS
    • A61P43/00—Drugs for specific purposes, not provided for in groups A61P1/00-A61P41/00

Definitions

  • the present invention relates to an agent for controlling Bcl-2 expression comprising ginsenoside F1 (20-O- ⁇ -D-glucopyranosyl-20(S)-protopanaxatriol) represented by the following formula 1 as an active component.
  • Ultraviolet radiation is a part of solar rays with 200-400 nm of wavelength and is a part of the electromagnetic spectrum; especially UVB (Ultraviolet-B) with 280-320 nm of wavelength is the major part of the ultraviolet radiation to cause skin aging leading to skin-burn and skin cancer.
  • UVB Ultraviolet-B
  • DNA, proteins, lipids, etc., in cells are damaged and thereby generate sunburn-cells.
  • These sunburn-cells undergo apoptosis, accompanied by DNA fragmentation, activation of caspase, and the like.
  • High-dose radiation on the cell causes serious DNA damages that are not recovered from; and the apoptosis prevents the cell from developing to a tumor by inducing the cell to die. Therefore, in order to prevent cancer and maintain cell homeostasis, it is very important to induce or to prevent apoptosis of the cell selectively according to the degree of cell damages.
  • Bcl-2 plays a very important role in the process of apoptosis of the skin cell.
  • the Bcl-2 gene encodes 26 kDa protein present in a nuclear membrane and an outer membrane of mitochondria.
  • Bcl-2 is a protein that inhibits apoptosis of a cell by adhering to a protein such as Bax, which accelerates the apoptosis, to inhibit its function. Therefore, apoptosis of a cell can be determined by the concentration ratio of Bcl-2 and Bax.
  • UVB irradiation has been known to decrease Bcl-2 expression of human keratinocyte. Furthermore, Bcl-2-transfected HaCaT cells or Bcl-2-overexpressing transgenic mice were shown to be resistant to UVB-induced apoptosis. However, over-expression of Bcl-2 prevents apoptosis of a cell with serious DNA damage and thereby causes a cancer. Therefore, it is very important to control the expression of Bcl-2 selectively.
  • Bcl-2 a type IV POU domain transcription factor
  • ginsenoside F1 which obtained from purified ginseng saponin, protects human HaCaT cells from UVB-induced apoptosis by maintaining constant levels of Bcl-2. That is, the present inventors found that ginsenoside F1 controls the expression of Bcl-2 and thereby inhibits the apoptosis of cells, and so accomplished the present invention.
  • an object of the present invention is to provide an agent for controlling Bcl-2 expression comprising ginsenoside F1 as an active component.
  • Another objection of the present invention is to provide a promoter or an inhibitor of apoptosis comprising ginsenoside F1 as an active component.
  • the present invention provides an agent for controlling Bcl-2 expression comprising ginsenoside F1 represented by the following formula 1 as an active component.
  • Ginsenoside F1 protects these cells against low-dose radiation of UVB-induced apoptosis by maintaining constant levels of Brn-3a and the corresponding inhibition of Bcl-2 downregulation. That is, ginsenoside F1 itself does not promote the Bcl-2 expression, but inhibits the downregulation of Bcl-2 caused by ultraviolet radiation. On the contrary, under the high-dose radiation of ultraviolet rays, it induces the decrease of Bcl-2 expression to promote apoptosis.
  • ginsenoside F1 inhibits the decrease of Bcl-2 expression under low-dose radiation of ultraviolet rays resultingly to prevent apoptosis of cells; however induces apoptosis under the high-dose radiation of ultraviolet rays, on the contrary; and thereby prevents skin cancer. Therefore, ginsenoside F1 may be used as an anti-aging material inhibiting cell damages.
  • the present invention confirmed that ginsenoside F1 controls the expression of Brn-3a, a transcription factor of Bcl-2, and thereby can maintain the degree of Bcl-2 expression to a normal level.
  • ginsenoside F1 can prevent apoptosis by maintaining the degree of Bcl-2 expression in a cell to desirable level.
  • ginsenoside F1 itself does not promote the Bcl-2 expression.
  • FIG. 1 is a graph showing viabilities of HaCaT skin cells obtained from the result of MTT assay, wherein cells treated with ginsenoside F1 and exposed to ultraviolet radiation were compared with a control (cells) untreated with ginsenoside F1.
  • FIG. 2 shows the changes of shapes of the cells, wherein cells treated with ginsenoside F1 and exposed to ultraviolet radiation were compared with a control untreated with ginsenoside F1.
  • FIG. 3 shows the degrees of DNA fragmentation of cells, wherein cells treated with ginsenoside F1 and exposed to ultraviolet radiation were compared with a control untreated with ginsenoside F1.
  • FIG. 4 shows the degrees of PARP segmentation in cells obtained from the result of Western blotting, wherein cells treated with ginsenoside F1 and exposed to ultraviolet radiation were compared with a control untreated with ginsenoside F1.
  • FIG. 5 shows the degrees of Bcl-2 expression with mRNA level, wherein cells treated with ginsenoside F1 and exposed to ultraviolet radiation were compared with a control untreated with ginsenoside F1.
  • FIG. 6 shows the degrees of the expression of Bm-3a, a transcription factor of Bcl-2, obtained from Western blotting, wherein cells treated with ginsenoside F1 and exposed to ultraviolet radiation were compared with a control untreated with ginsenoside F1.
  • Hsp 70 means that a same amount of protein was used.
  • the extract (1-butanol extract) was dissolved in a small amount of methanol, and a large amount of ethylacetate was added thereto to obtain precipitation.
  • the precipitation was dried to obtain 70 g of purified ginseng saponin extract.
  • Human keratinocyte, HaCaT obtained from Dr. Fusenig in German Cancer Research Center (DKFZ) was cultured in Dulbecco's modified Eagle's Medium (DMEM; Gibco 1210-0038) containing 10% of fetal bovin serum at 37° C. and 5% of CO 2 .
  • DMEM Dulbecco's modified Eagle's Medium
  • step 1 Cells cultured in step 1 were treated with trypsin to obtain single cell suspension, and seeded into 6-well flask with 2 ⁇ 10 5 /well, then cultured for 24 hours. After that, the cells were cultured again in a new DMEM not containing fetal bovin serum for 24 hours, then treated with 1, 5, 10 ⁇ M of ginsenoside F1. Ginsenoside F1 was dissolved in 100% ethanol and added to be 1/1000 of the medium concentration. After 24 hours of treatment with ginsenoside F1, the cell cultures were washed with phosphate buffered saline (PBS), and exposed to 60-120 mJ/cm 2 of UVB radiation with a state containing PBS.
  • PBS phosphate buffered saline
  • the PBS was removed and medium was changed with a fresh one containing the same concentration of ginsenoside F1.
  • the cells untreated with ginsenoside F1 were cultured as a control.
  • 3-[4,5-dimethyl tetrazole]-2,5-diphenyltetrazolium bromide (MTT, Sigma) was added to all the cells treated and untreated with ginsenoside F1, then cultured 4 hours at 37° C. After culture, the cells were dissolved with dimethylsulfoxide, then optical density (OD) of formazan dye generated at 540 nm was measured with ELISA reader (Thermo Max, Molecular Devices Co.).
  • OD value of the cells not-exposed to the UVB was given 100%, then the relative values of the other cells were calculated and determined as viabilities thereof.
  • the results are shown in FIG. 1 .
  • the cells treated with ginsenoside F1 showed 1.5 times more inhibition of apoptosis compared with those untreated, when exposed to the UVB. However, under the 120 mJ/cm 2 of UVB radiation, the cells treated with ginsenoside F1 showed more apoptosis than those untreated.
  • step 1 Cells cultured in step 1 were treated with trypsin to obtain single cell suspension, and seeded into 6-well flask with 2 ⁇ 10 5 /well, then cultured for 24 hours. After that the cells were cultured again in a new DMEM not containing fetal bovin serum for 24 hours, then treated with 5 ⁇ M of ginsenoside F1. After 24 hours of treatment with ginsenoside F1, the cultures were washed with phosphate buffered saline (PBS), and exposed to 60 mJ/cm 2 of UVB radiation with a state containing PBS. Then, the PBS was removed and medium was changed with a fresh one containing the same concentration of ginsenoside F1. In addition, the cells untreated with ginsenoside F1 were cultured as a control.
  • PBS phosphate buffered saline
  • Reaction termination buffer TUNEL Apoptosis detection kit, Upstate, USA
  • blocking solution TUNEL Apoptosis detection kit, Upstate, USA
  • Avidin-FITC TUNEL Apoptosis detection kit, Upstate, USA
  • step 1 Cells cultured in step 1 were treated with trypsin to obtain single cell suspension, and seeded into 6-well flask with 2 ⁇ 10 5 /well, then cultured for 24 hours. After that the cells were cultured again in a new DMEM not containing fetal bovin serum for 24 hours, then treated with 5 ⁇ M of ginsenoside F1. After 24 hours of treatment with ginsenoside F1, the cell cultures were washed with phosphate buffered saline (PBS), and exposed to 60 mJ/cm 2 of UVB radiation with a state containing PBS. Then, the PBS was removed and medium was changed with a fresh one containing 5 ⁇ M of ginsenoside F1. In addition, the cells untreated with ginsenoside F1 were cultured as a control.
  • PBS phosphate buffered saline
  • the blots reacted were exposed to X-ray Fuji film and developed to observe the degree of protein expression. Bands on the film were scanned with PowerLook 2100 XL (umax) and analyzed with an image-analyzing program of ImageMaster 2D Elite (Amersham Bioscience). The amount of PARP protein segmentation was estimated with a relative value compared with that of control. The cells treated with ginsenoside F1 showed 1.4 times decrease of PARP protein segmentation compared with those untreated, when exposed to the UVB. The results are shown in FIG. 4 .
  • step 1 Cells cultured in step 1 were treated with trypsin to obtain single cell suspension, and seeded into 6-well flask with 2 ⁇ 10 5 /well then cultured for 24 hours. After that the cells were cultured again in a new DMEM not containing fetal bovin serum for 24 hours, then treated with 5 ⁇ M of ginsenoside F1. After 24 hours of treatment with ginsenoside F1, the cell cultures were washed with phosphate buffered saline (PBS), and exposed to 60 mJ/cm 2 of UVB radiation with a state containing PBS. Then, the PBS was removed and medium was changed with a fresh one containing 5 ⁇ M of ginsenoside F1. In addition, the cells untreated with ginsenoside F1 were cultured as a control.
  • PBS phosphate buffered saline
  • Bcl-2 and GAPDH primers to performed quantitative RT-PCR Primer Sequence Bcl-2 forward primer 5′-TACGATAACCGGGAGATAGTGA-3′ (nucleotides 56-77 of human Bcl-2 cDNA)
  • Bcl-2 reverse Primer 5′-CAGGTGCCGGTTCAGGTACT-3′ (nucleotides 566-586 of human Bcl-2 cDNA)
  • GAPDH forward primer 5′-CAACTACATGGTTTACATGTTCC-3′ (nucleotides 174-194 of human GAPDH cDNA)
  • GAPDH reverse primer 5′-GGACTGTGGTCATGAGTCCT-3′ (nucleotides 570-589 of human GAPDH cDNA)
  • PCR buffer solution 2.5 ⁇ l of reverse transcription reaction solution was mixed to 50 ⁇ l PCR buffer solution with 50 mM of KCl, 10 mM of tris-HCl (pH 8.3), 5 mM of MgCl 2 and 100 ⁇ M of dNTP, and 10 ⁇ M of primer and 0.5U of Taq DNA polymerase were added thereto, then repeated 30 cycles of; 30 sec at 95° C., 30 sec at 58° C. and 30 sec at 72° C. PCR products were electrophoresed through agarose gels and scanned, then analyzed with the image-analyzing program of ImageMaster 2D Elite (Amersham Bioscience). The degree of Bcl-2 expression was estimated with a relative value compared with that of GAPDH.
  • step 1 Cells cultured in step 1 were treated with trypsin to obtain single cell suspension, and seeded into 6-well flask with 2 ⁇ 10 5 /well, then cultured for 24 hours. After that the cells were cultured again in a new DMEM not containing fetal bovin serum for 24 hours, then treated with 5 ⁇ M of ginsenoside F1. After 24 hours of treatment with ginsenoside F1, the cell cultures were washed with phosphate buffered saline (PBS), and exposed to 60 mJ/cm 2 of UVB radiation with a state containing PBS. Then, the PBS was removed and medium was changed with a fresh one containing 5 ⁇ M of ginsenoside F1. In addition, the cells that are not treated with ginsenoside F1 were cultured as a control.
  • PBS phosphate buffered saline
  • ginsenoside F1 of the present invention inhibits the decrease of Bcl-2 expression caused by ultraviolet radiation to inhibit apoptosis induced from ultraviolet radiation, on the contrary under the high-dose ultraviolet radiation, ginsenoside F1 promotes apoptosis of cell to prevent the cell from developing as a cancer cell.

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US10/539,012 2002-12-28 2003-12-27 Agent for controlling bcl-2 expression comprising ginsenoside f1 as an active component Abandoned US20070155829A1 (en)

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US12/135,663 US8258272B2 (en) 2002-12-28 2008-06-09 Agent for controlling Bcl-2 expression comprising ginsenoside F1 as an active component

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KR10-2002-0085716 2002-12-28
KR1020020085716A KR100820072B1 (ko) 2002-12-28 2002-12-28 진세노사이드 Ｆ1을 유효성분으로 하는 Ｂｃｌ-2 발현조절제
PCT/KR2003/002859 WO2004058141A2 (fr) 2002-12-28 2003-12-27 Agent destine a reguler l'expression de bcl-2, contenant du ginsenoside f1 en tant qu'ingredient actif

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TW200804336A (en) 2006-03-23 2008-01-16 Actelion Pharmaceuticals Ltd Cyclohexyl or piperidinyl carboxamide antibiotic derivatives
ES2634232T3 (es) 2007-10-31 2017-09-27 Amorepacific Corporation Uso de inhibidores de biosíntesis de melanina a partir de ginseng para el blanqueo de la piel
WO2012031103A2 (fr) * 2010-09-01 2012-03-08 Case Western Reserve University Inhibiteurs de bcl-2
KR101777920B1 (ko) * 2015-07-27 2017-09-14 재단법인 지능형 바이오 시스템 설계 및 합성 연구단 진세노사이드 f1을 포함하는 아밀로이드 플라크 제거용 조성물

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FR2695561B1 (fr) 1992-09-17 1994-12-02 Lvmh Rech Gie Composition cosmétique ou dermatologique contenant au moins une saponine de type ginsenoside, et ses applications, notamment pour le soin des cheveux.
US6001992A (en) * 1999-01-07 1999-12-14 Isis Pharmaceuticals Inc. Antisense modulation of novel anti-apoptotic bcl-2-related proteins
JP3193542B2 (ja) * 1993-09-08 2001-07-30 カネボウ株式会社 皮膚老化防止化粧料
KR100192678B1 (ko) * 1995-06-07 1999-06-15 손경식 약효가 증강된 가공인삼 제품
JP2001511344A (ja) * 1997-07-25 2001-08-14 ニューロヴェックス リミテッド 転写因子Ｂｒｎ−３ａの使用
KR100361433B1 (ko) * 1998-05-28 2003-01-24 주식회사 태평양 인삼추출물을함유하는피부노화방지용화장료조성물
US6261603B1 (en) * 1999-05-11 2001-07-17 Mcelwain Elizena A. Skin cream
KR100418604B1 (ko) * 2001-11-01 2004-02-11 주식회사 태평양 인삼 사포닌으로부터 화합물 ｋ 및 진세노사이드 ｆ1을제조하는 방법
JP4549625B2 (ja) * 2002-01-05 2010-09-22 株式會社アモーレパシフィック 人参サポニン代謝産物を有効成分とする微細乳化粒子及びその製造方法、並びにこれを含有する皮膚老化防止用の化粧料組成物
KR100465976B1 (ko) * 2002-01-05 2005-01-13 주식회사 태평양 나노유화기술에 의해 진세노사이드 ｆ1을 함유하는 미세 유화 입자 및 이를 사용한 피부 외용제 조성물
KR100835864B1 (ko) * 2002-05-27 2008-06-09 (주)아모레퍼시픽 인삼사포닌 대사 산물을 유효 성분으로 한 미세 유화 입자 및 그 제조방법, 이를 함유한 피부 노화방지용 화장료 조성물

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AU2003289538A1 (en) 2004-07-22
JP2006512384A (ja) 2006-04-13
KR20040059139A (ko) 2004-07-05
US20080261899A1 (en) 2008-10-23
US8258272B2 (en) 2012-09-04
CN100404034C (zh) 2008-07-23
WO2004058141A2 (fr) 2004-07-15
JP4654040B2 (ja) 2011-03-16
WO2004058141A3 (fr) 2004-12-02
EP1575599A2 (fr) 2005-09-21
KR100820072B1 (ko) 2008-04-10
AU2003289538A8 (en) 2004-07-22
CN1732010A (zh) 2006-02-08

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