首页> 外国专利> METHOD FOR PRODUCING NOVEL GYNOSTEMMA PENTAPHYLLUM EXTRACTS HAVING INCREASED AMOUNTS OF DAMULIN A AND DAMULIN B AND PHARMACEUTICAL COMPOSITION FOR TREATING METABOLIC DISEASES USING THE SAME

METHOD FOR PRODUCING NOVEL GYNOSTEMMA PENTAPHYLLUM EXTRACTS HAVING INCREASED AMOUNTS OF DAMULIN A AND DAMULIN B AND PHARMACEUTICAL COMPOSITION FOR TREATING METABOLIC DISEASES USING THE SAME

机译：生产含量增加的DAMULIN A和DAMULIN B的新的绞股蓝提取物的方法以及使用相同的药物治疗代谢性疾病的药物组合物

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摘要

The present invention relates to a use of an AMP-activated protein kinase (AMPK) activator for relieving and treating metabolic diseases wherein AMPK is an energy sensor and key enzyme for regulating lipid and glucose metabolism in a living body. When AMPK is activated, synthesis of lipid and cholesterol is inhibited; body fat is decreased; lowering of blood glucose is facilitated; and obesity, diabetes, and hyperlipidemia are relieved. In the present invention, novel compounds Damulin A (2α,3â,12â-trihydroxydammar-20(22)-E,24-diene-3-O-[â-D-glucopyranosyl-(1→)-â-D-glucopyranoside]) and Damulin B (2α,3â,12â-trihydroxydammara-20,24-diene-3-O-[â-D-glucopyranosyl-(1→)-â-D-glucopyranoside]) are used as the AMPK activator for the active ingredients for relieving and treating metabolic diseases including obesity, diabetes, and hyperlipidemia. In addition, the present invention provides a method for increasing the amount of Damulin A or Damulin B which is the valid indicator for AMPK activation by treating Gynostemma pentaphyllum extracts at high temperature and high pressure. Therefore, the present invention also provides a use of novel Gynostemma pentaphyllum extracts with remarkably increased capacity of activating AMPK for relieving or treating metabolic diseases such as obesity, diabetes, and hyperlipidemia.

机译：本发明涉及一种AMP活化的蛋白激酶（AMPK）活化剂在缓解和治疗代谢疾病中的用途，其中AMPK是一种能量传感器和用于调节生物体内脂质和葡萄糖代谢的关键酶。激活AMPK后，脂质和胆固醇的合成受到抑制;体内脂肪减少;有助于降低血糖;肥胖，糖尿病和高脂血症得到缓解。在本发明中，新化合物Damulin A（2 α，3â，12âI>- trihydroxydammar-20（22）- E ，24-diene -3- O- [â- D-吡喃葡萄糖基-（1→）-â- D-吡喃葡萄糖苷]）和Damulin B（2 α，3â，12âI>- trihydroxydammara-20,24-diene-3- O- [â-D-glucopyranosyl-（1→） -β-D-吡喃葡萄糖苷]）用作有效成分的AMPK活化剂，可减轻和治疗包括肥胖，糖尿病和高脂血症在内的代谢疾病。另外，本发明提供了一种通过在高温高压下处理绞股蓝绞股蓝提取物来增加作为激活AMPK的有效指标的达木林A或达木林B的量的方法。因此，本发明还提供了具有显着增加的激活AMPK的能力的新型绞股蓝绞股蓝提取物在缓解或治疗代谢性疾病如肥胖，糖尿病和高脂血症中的用途。 展开▼

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公开/公告号WO2011007943A1

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公开/公告日2011-01-20

原文格式PDF

申请/专利权人 TG BIOTECH CO. LTD.;HUH TAE LIN;SONG HE BOK;KIM JI EUN;JOON SO YOUNG;OH WON KEUN;
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申请/专利号WO2009KR07668

发明设计人 HUH TAE LIN;SONG HE BOK;KIM JI EUN;JOON SO YOUNG;OH WON KEUN;
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申请日2009-12-22

分类号A61K36/424;A61P3/04;A61P3/10;A23L1/30;

国家 WO

入库时间 2022-08-21 17:59:49

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1. 达木林A及达木林B含量增加的新绞股蓝提取物制备方法及利用该提取物制备的代谢疾病治疗用药物组合物 [P] . 中国专利： CN102470155B . 2014.10.08

2. 达木林A及达木林B含量增加的新绞股蓝提取物制备方法及利用该提取物制备的代谢疾病治疗用药物组合物 [P] . 中国专利： CN102470155A . 2012-05-23

3. Method for preparing Gynostemma pentaphyllum extract with increasing damulin A and damulin B contents, and pharmaceutical compositions of the same for treating metabolic disease [P] . 美国专利： US8357786B2 . 2013-01-22

机译：一种增加大青素A和大青素B含量的绞股蓝绞股蓝提取物的制备方法及用于治疗代谢性疾病的药物组合物

4. METHOD FOR PREPARING GYNOSTEMMA PENTAPHYLLUM EXTRACT WITH INCREASING DAMULIN A AND DAMULIN B CONTENTS, AND PHARMACEUTICAL COMPOSITIONS OF THE SAME FOR TREATING METABOLIC DISEASE [P] . 美国专利： US2011015142A1 . 2011-01-20

机译：增高达木林A和达木林B含量的制备雌雄同体五倍体提取物的方法以及用于治疗代谢性疾病的相同药物成分

5. THE METHOD FOR PREPARING GYNOSTEMMA PENTAPHYLLUM EXTRACT WITH INCREASING DAMULIN A AND DAMULIN B CONTENTS, AND A PHARMACEUTICAL COMPOSITIONS OF THE SAME FOR TREATING METABOLIC DISEASE [P] . 韩国专利： KR100930580B1 . 2009-12-09

机译：增高达木林A和达木林B含量的制备雌雄同体提取物的方法以及用于治疗代谢性疾病的相同药物成分

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4. Neuroprotective Effects of Herbal Ethanol Extracts from Gynostemma pentaphyllum in the 6-Hydroxydopamine-Lesioned Rat Model of Parkinsons Disease [O] . Hyun Sook Choi, Mi Sook Park, Seung Hwan Kim, 2010

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Vascular304Mitophagy acts as a safeguard mechanism against human vascular smooth muscle cell apoptosis induced by atherogenic lipidsTranscriptional control and RNA species - Vascular307MicroRNA-34a role in vascular calcification308Local delivery of a miR-146a inhibitor utilizing a clinically applicable approach attenuates neointima formation after vascular injury309Long noncoding RNA landscape of hypoxic endothelial cells310Specific circulating microRNAs levels associate with hypertension, hyperglycemia and dysfunctional HDL in acute coronary syndrome patientsCytokines and cellular inflammation - Vascular313Phosphodiesterase5A up-regulation in vascular endothelium under pro-inflammatory conditions: a newly disclosed anti-inflammatory activity for the omega-3polyunsaturated aatty acid docosahexaenoic acid314Cardiovascular risk modifying with extra-low dose anticytokine drugs in rhematoid arthritis315Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation316Lymphocytic myocarditis coincides with increased plaque inflammation and plaque hemorrhage in coronary arteries, facilitating myocardial infarction317Serum osteoprotegerin level predictsdeclined numerous of circulating endothelial- derived and mononuclear-derived progenitor cells in patients with metabolic syndromeGrowth factors and neurohormones - Vascular320Effect of gastrin-releasing peptide (GRP) on vascular inflammationSignal transduction - Heart323A new synthetic peptide regulates hypertrophy in vitro through means of the inhibition of nfkb324Inducible fibroblast-specific knockout of p38 alpha map kinase is cardioprotective in a mouse model of isoproterenol-induced cardiac hypertrophy325Regulation of beta-adrenoceptor-evoked inotropic responses by inhibitory G protein, adenylyl cyclase isoforms 5 and 6 and phosphodiesterases326Binding to RGS3 and stimulation of M2 muscarinic acetylcholine receptors modulates the substrate specificity of p190RhoGAP in cardiac myocytes327Cardiac regulation of post-translational modifications, parylation and deacetylation in LMNA dilated cardiomyopathy mouse model328Beta-adrenergic regulation of the b56delta/pp2a holoenzyme in cardiac myocytes through b56delta phosphorylation at serine 573Nitric oxide and reactive oxygen species - Vascular331Oxidative stress-induced miR-200c disrupts the regulatory loop among SIRT1, FOXO1 and eNOS332Antioxidant therapy prevents oxidative stress-induced endothelial dysfunction and Enhances Wound Healing333Morphological and biochemical characterization of red blood cell in coronary artery diseaseCytoskeleton and mechanotransduction - Heart336Novel myosin activator, JSH compounds, increased myocardial contractility without chronotropic effect in ratsExtracellular matrix and fibrosis - Vascular339Ablation of Toll-like receptor 9 causes cardiac rupture after myocardial infarction by attenuating proliferation and differentiation of cardiac fibroblasts340Altered vascular remodeling in the mouse hind limb ischemia model in Factor VII activating protease (FSAP) deficiencyVasculogenesis, angiogenesis and arteriogenesis343Pro-angiogenic effects of proly-hydroxylase inhibitors and their potential for use in a novel strategy of therapeutic angiogenesis for coronary total occlusion344Nrf2 drives angiogenesis in transcription-independent manner: new function of the master regulator of oxidative stress response345Angiogenic gene therapy, despite efficient vascular growth, is not able to improve muscle function in normoxic or chronically ischemic rabbit hindlimbs -role of capillary arterialization and shunting346Effect of PAR-1 inhibition on collateral vessel growth in the murine hind limb model347Quaking is a key regulator of endothelial cell differentiation, neovascularization and angiogenesis348"Emerging angiogenesis" in the chick chorioallantoic membrane (CAM). 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