1. Metabolic Enzyme/Protease Apoptosis Anti-infection Cell Cycle/DNA Damage Immunology/Inflammation GPCR/G Protein NF-κB PI3K/Akt/mTOR
  2. MMP Apoptosis HSV DNA/RNA Synthesis NO Synthase Prostaglandin Receptor Reactive Oxygen Species (ROS) Akt
  3. 20(R)-Ginsenoside Rh2

20(R)-Ginsenoside Rh2  (Synonyms: 20(R)-人参皂苷Rh2)

目录号: HY-N1401 纯度: 99.84%
COA 产品使用指南 技术支持

20(R)-Ginsenoside Rh2 是一种口服有效的、具备多种生物活性的原人参二醇型皂苷。20(R)-Ginsenoside Rh2 通过诱导细胞周期阻滞、促进凋亡 (apoptosis) 对非小细胞肺癌、肝癌具有显著抑制作用。20(R)-Ginsenoside Rh2 能通过抑制病毒 DNA 复制发挥抗 γ-疱疹病毒作用。20(R)-Ginsenoside Rh2 降低一氧化氮 (NO) 、前列腺素 E2 (PGE2) 和活性氧 (ROS) 水平抑制炎症介质,通过减少 ROS 和抑制 MMP-9/2,可延缓皮肤光老化。20(R)-Ginsenoside Rh2 通过激活 Akt1/PKB 信号通路,加速肌肉损伤后的恢复。20(R)-Ginsenoside Rh2 可抑制破骨细胞形成发挥抗骨质疏松作用。

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20(R)-Ginsenoside Rh2

20(R)-Ginsenoside Rh2 Chemical Structure

CAS No. : 112246-15-8

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Other Forms of 20(R)-Ginsenoside Rh2:

MCE 顾客使用本产品发表的 1 篇科研文献

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

20(R)-Ginsenoside Rh2 is an orally active protopanaxadiol-type saponin with multiple biological activities. 20(R)-Ginsenoside Rh2 exerts a significant inhibitory effect on non-small cell lung cancer and liver cancer by inducing cell cycle arrest and promoting apoptosis. 20(R)-Ginsenoside Rh2 exerts anti-γ-herpesvirus effects by inhibiting viral DNA replication. 20(R)-Ginsenoside Rh2 inhibits inflammatory mediators by reducing the levels of NO, PGE2, and ROS; it can delay skin photoaging by reducing ROS and inhibiting MMP-9/2 activity. 20(R)-Ginsenoside Rh2 accelerates the recovery after muscle injury by activating the Akt1/PKB signaling pathway. 20(R)-Ginsenoside Rh2 can inhibit osteoclast formation and exert an anti-osteoporosis effect[1][2][3][4][5][6].

IC50 & Target[1][5]

MMP9

 

MMP2

 

Akt1

 

体外研究
(In Vitro)

20(R)-Ginsenoside Rh2 (0-50 μM, 24 h) 能够抑制 NO、PGE2、ROS 和 MMP-9 (基质金属蛋白酶-9) 的产生,但不能调节由 LPS (HY-D1056) 在 RAW264.7 巨噬细胞中诱导的 MMP-2 (基质金属蛋白酶-2) 的明胶酶活性[1]
20(R)-Ginsenoside Rh2 (0-25 μM, 24 h) 降低 ROS 水平 (但不能调节 NO),抑制未受刺激的 HaCat 细胞中 MMP-9MMP-2 的明胶酶活性,且对 HaCat 细胞无细胞毒性[1]
20(R)-Ginsenoside Rh2 (0-200 μg/mL, 24 h-28 d) 抑制 95D 和 NCI-H460 细胞的增殖和集落形成,并诱导这两种细胞凋亡[3]
20(R)-Ginsenoside Rh2 (50-100 μg/mL, 48 h) 介导 95D 细胞的 G1/S 期细胞周期阻滞和 NCI-H460 细胞的 G2 期细胞周期阻滞[3]
20(R)-Ginsenoside Rh2 (0-100 μM, 72 h) 通过抑制 MHV-68 进入 NIH-3T3 细胞后的复制,显著抑制小鼠 γ 疱疹病毒68 (MHV-68) 的增殖 (IC50 = 2.77 μM),且抑制人 γ 疱疹病毒 (KSHV) 阳性细胞系 BC3 的裂解复制[4]
20(R)-Ginsenoside Rh2 (5-10 μg/mL, 72 h) 通过激活 Akt/PKB 信号通路并抑制 p27Kip1 和 p57KIP2 的表达,增加 C2C12 小鼠成肌细胞的增殖并抑制原代大鼠心肌细胞的增殖[5]
20(R)-Ginsenoside Rh2 对破骨细胞形成有抑制作用 (IC50 = 12 μM),对破骨细胞增殖无抑制作用[6]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[1]

Cell Line: HaCat cells
Concentration: 0, 0.2, 1, 5 and 25 μM
Incubation Time: 24 h
Result: Observed the reduction of MMP-9 and MMP-2 gelatinolytic activity.
Inhibited TNF-a-induced MMP-9 gelatinolytic activity.

Cell Proliferation Assay[3]

Cell Line: 95D and NCI-H460 cells
Concentration: 0, 50, 100, 200 µg/mL
Incubation Time: 24, 48 and 72 h
Result: Exhibited the IC50s of 1006.15, 491.46 and 596.81 µg/mL at 24, 48 and 72 h against 95D cells.
Exhibited the IC50s of 386,77, 783,49 and 368,32 µg/mL at 24, 48 and 72 h against NCI-H460 cells.

Cell Cycle Analysis[3]

Cell Line: 95D and NCI-H460 cells
Concentration: 50 and 100 µg/mL
Incubation Time: 48 h
Result: Increased the accumulation rate of 95D cells in S phase from 34.70% to 43.05% and that of NCI‑H460 cells in S phase is 3.64% to 22.94% at 100 µg/mL.

Apoptosis Analysis[3]

Cell Line: 95D and NCI-H460 cells
Concentration: 50 and 100 µg/mL
Incubation Time: 48 h
Result: Had the maximum total apoptosis rate of 21.67% in 95D cells and NCI‑H460 cells total apoptosis rate was 27.30%.
The number of nuclear fragmentation (apoptotic bodies) has significantly increased.

RT-PCR[4]

Cell Line: NIH-3T3 cells infected MHV-68
Concentration: 100 µM
Incubation Time: 72 h
Result: Reduced the mRNA expression of the viral lysate gene RTA.
Reduced the expression of the RTA (key gene during the lytic phase) and ORF56 (gene related to DNA synthesis).

Western Blot Analysis[4]

Cell Line: NIH-3T3 cells infected MHV-68
Concentration: 100 µM
Incubation Time: 72 h
Result: Significantly decreased the expression of the late viral protein ORF45 (capsid protein) and M9.

Immunofluorescence[5]

Cell Line: C2C12 murine myoblasts
Concentration: 5 and 10 µg/mL
Incubation Time: 72 h
Result: Selectively enhanced myoblast proliferation (BrdU of human primary cells increased by 35%).
Inhibited the proliferation of cardiac fibroblasts (CdF).

RT-PCR[5]

Cell Line: C2C12 myoblast cells and primary rat cardiomyocytes
Concentration: 5 µg/mL
Incubation Time: 72 h
Result: Significantly downregulated p27Kip1 and p57Kip2 mRNA in C2C12 myoblast cells.
Downregulated p27Kip1 and showed no change on p57Kip2 in primary rat cardiomyocytes.

Western Blot Analysis[5]

Cell Line: C2C12 myoblast cells and primary rat cardiomyocytes
Concentration: 5 and 10 µg/mL
Incubation Time: 72 h
Result: Significantly increased Akt phosphorylation in C2C12 myoblast cells.
Consistented with the mRNA results.
体内研究
(In Vivo)

20(R)-Ginsenoside Rh2 (2-6 mg/kg, p.o., 每日一次共 10 天) 通过下调 Bcl-2 诱导肿瘤细胞凋亡,在小鼠肝癌模型中发挥了显著的抗肿瘤效果[2]
20(R)-Ginsenoside Rh2 (2 mg/kg, i.p., 每日一次共 7 天) 可促进心肌梗死大鼠模型中心肌细胞的增殖并改善心脏功能[5]
20(R)-Ginsenoside Rh2 (2 mg/kg, i.p., 每日一次共 7-14 天) 可加速骨骼肌退化小鼠模型中骨骼肌的再生并减少纤维化[5]
20(R)-Ginsenoside Rh2 (5 μg/mL) 可增强斑马鱼心肌细胞的增殖[5]

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Myocardial infarction model established in adult male 8-week-old Sprague Dawley rats (weight range 230-250 g)[5]
Dosage: 2 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily, for 7 days
Result: Increased ejection fraction (EF) by 28%, left ventricular wall thickness increased, and scar area decreased.
Animal Model: Hepatoma model established in female H22 hepatoma-bearing mice (18-22g)[2]
Dosage: 2, 3, 4, 6mg/kg
Administration: Oral administration (p.o.), once daily for 10 days
Result: Significantly inhibited tumor growth, and the weight of the mice remained stable.
The number of nuclear divisions decreased, the area of necrosis increased, and apoptotic-like cells (with nuclear shrinkage and fragmentation) were significantly present.
Significantly downregulated the expression of Bcl-2, Bax/Bak/Bcl-xL, but no significant change was observed.
Animal Model: Skeletal muscle degeneration model established in 8-week-old male C57BL/6 mice (weight range 23-25 g) [5]
Dosage: 2 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily, for 7 and 14 days
Result: Observed a large number of central nuclear myofibers (indicative of new formation) with their diameters significantly increased compared to the control group during 7 days treatment.
The number of inflammatory cells decreased by 50% during 7 days treatment.
Arranged more closely in the muscle fibers, reduced the scar area, and the swimming time remained stable during 14 days treatment.
分子量

622.87

Formula

C36H62O8

CAS 号
性状

固体

颜色

White to off-white

中文名称

20(R)-人参皂苷Rh2

结构分类
初始来源
运输条件

Room temperature in continental US; may vary elsewhere.

储存方式

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

溶解性数据
细胞实验: 

DMSO 中的溶解度 : 100 mg/mL (160.55 mM; 超声助溶; 吸湿的 DMSO 对产品的溶解度有显著影响,请使用新开封的 DMSO)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.6055 mL 8.0274 mL 16.0547 mL
5 mM 0.3211 mL 1.6055 mL 3.2109 mL
查看完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C储存时,请在6个月内使用,-20°C储存时,请在1个月内使用。

  • 摩尔计算器

  • 稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量
=
浓度
×
体积
×
分子量 *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start)

C1

×
体积 (start)

V1

=
浓度 (final)

C2

×
体积 (final)

V2

动物实验:

请根据您的 实验动物和给药方式 选择适当的溶解方案。

以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液,再依次添加助溶剂:
——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议您现用现配,当天使用
以下溶剂前显示的百分比是指该溶剂在您配制终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶

  • 方案 一

    请依序添加每种溶剂: 10% DMSO    90% Corn Oil

    Solubility: ≥ 2.5 mg/mL (4.01 mM); 澄清溶液

    此方案可获得 ≥ 2.5 mg/mL(饱和度未知)的澄清溶液,此方案实验周期在半个月以上的动物实验酌情使用。

    1 mL 工作液为例,取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中,混合均匀。

动物溶解方案计算器
请输入动物实验的基本信息:

给药剂量

mg/kg

动物的平均体重

g

每只动物的给药体积

μL

动物数量

由于实验过程有损耗,建议您多配一只动物的量
请输入您的动物体内配方组成:
%
DMSO +
+
%
Tween-80 +
%
Saline
如果您的动物是免疫缺陷鼠或者体弱鼠,建议 DMSO 中的在最后工作液体系中的占比尽量不超过 2%。
方案所需 助溶剂 包括:DMSO ,均可在 MCE 网站选购。 Tween 80,均可在 MCE 网站选购。
计算结果
工作液所需浓度 : mg/mL
储备液配制方法 : mg 药物溶于 μL  DMSO(母液浓度为 mg/mL)。

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

您所需的储备液浓度超过该产品的实测溶解度,以下方案仅供参考,如有需要,请与 MCE 中国技术支持联系。
动物实验体内工作液的配制方法 : 取 μL DMSO 储备液,加入 μL  μL ,混合均匀至澄清,再加 μL Tween 80,混合均匀至澄清,再加 μL 生理盐水
连续给药周期超过半月以上,请谨慎选择该方案。
请确保第一步储备液溶解至澄清状态,从左到右依次添加助溶剂。您可采用超声加热 (超声清洗仪,建议频次 20-40 kHz),涡旋吹打等方式辅助溶解。
纯度 & 产品资料

纯度: 99.84%

参考文献

完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效
储备液的保存方式和期限:-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C储存时,请在6个月内使用,-20°C储存时,请在1个月内使用。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 1.6055 mL 8.0274 mL 16.0547 mL 40.1368 mL
5 mM 0.3211 mL 1.6055 mL 3.2109 mL 8.0274 mL
10 mM 0.1605 mL 0.8027 mL 1.6055 mL 4.0137 mL
15 mM 0.1070 mL 0.5352 mL 1.0703 mL 2.6758 mL
20 mM 0.0803 mL 0.4014 mL 0.8027 mL 2.0068 mL
25 mM 0.0642 mL 0.3211 mL 0.6422 mL 1.6055 mL
30 mM 0.0535 mL 0.2676 mL 0.5352 mL 1.3379 mL
40 mM 0.0401 mL 0.2007 mL 0.4014 mL 1.0034 mL
50 mM 0.0321 mL 0.1605 mL 0.3211 mL 0.8027 mL
60 mM 0.0268 mL 0.1338 mL 0.2676 mL 0.6689 mL
80 mM 0.0201 mL 0.1003 mL 0.2007 mL 0.5017 mL
100 mM 0.0161 mL 0.0803 mL 0.1605 mL 0.4014 mL
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