Rehmannioside A是细胞色素P450酶（CYP3A4、2C9和2D6）的抑制剂，IC50值分别为10.08、12.62和16.43μM。
Cas No.:81720-05-0
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
Rehmannioside A is an inhibitor of cytochrome P450 enzymes (CYP3A4, 2C9, and 2D6), with IC50 values of 10.08, 12.62, and 16.43μM, respectively[1]. Rehmannioside A is an iridoid glycoside isolated from Rehmanniae radix, possessing various biological activities including anti-inflammatory, antioxidant, anti-apoptotic, and neuroprotective effects[2, 3].
In vitro, treatment of mouse osteoblast cell lines (MC3T3-E1 cells) with Rehmannioside A (10-300µM) for 24h significantly improved the survival rate of dexamethasone-exposed osteoblasts at 50-200µM, and promoted the activation of the PI3K/AKT signaling pathway in MC3T3-E1 cells[4]. Treatment of HK2 cells with Rehmannioside A (20-80µM) for 24h significantly improved the survival rate of high glucose (HG)-induced HK2 cells, inhibited apoptosis and oxidative stress, and suppressed the activation of the intracellular MAPK pathway[5].
In vivo, Rehmannioside A (40, 80mg/kg) administered intraperitoneally to rats with vascular dementia (VD) for 14 days dose-dependently reduced the overexpression of TUNEL-positive cells, active Caspase-3, PARP, and cytochrome c in the hippocampus[6]. Oral administration of Rehmannioside A (5, 15, 45mg/kg) to 5×FAD mice significantly improved learning, memory, and cognitive function, reduced the accumulation of Aβ plaques in the hippocampus, reduced the number of microglia, increased the expression of PSD 95 and synaptophysin-1 proteins, and alleviated oxidative stress and inflammation[7].
References:
[1] Wang C, Zhou N, Li M, et al. Rehmannioside A inhibits the activity of CYP3A4, 2C9 and 2D6 in vitro[J]. Xenobiotica, 2024, 54(4): 195-200.
[2] Zhao K, Zhu H, Zheng L, et al. Harnessing the multi-targeted potential of rehmanniae radix natural products against renal fibrosis: a mechanistic review[J]. Frontiers in Pharmacology, 2025, 16: 1690036.
[3] Zhong H Z, Mo J, Li Y X, et al. Changes in Rehmanniae Radix processing and their impact on ovarian hypofunction: potential mechanisms of action[J]. Frontiers in pharmacology, 2024, 15: 1426972.
[4] Huang H, Ji F, Qi G, et al. Rehmannioside A promotes the osteoblastic differentiation of MC3T3-E1 cells via the PI3K/AKT signaling pathway and inhibits glucocorticoid-induced bone loss in vivo[J]. Journal of Pharmacological Sciences, 2024, 156(4): 247-257.
[5] Huai L, Yang L, Xu Q, et al. Rehmannioside A protects against high glucose-induced apoptosis and oxidative stress of renal tubular epithelial cells by inhibiting the MAPK pathway[J]. Tropical Journal of Pharmaceutical Research, 2021, 20(8): 1553-1558.
[6] Sun M, Shen X, Ma Y. Rehmannioside A attenuates cognitive deficits in rats with vascular dementia (VD) through suppressing oxidative stress, inflammation and apoptosis[J]. Biomedicine & Pharmacotherapy, 2019, 120: 109492.
[7] Lai Y, Zhao H. Therapeutic efficacy of rehmannioside A on 5× FAD mice in Alzheimer’s disease[J]. Scientific Reports, 2025, 15(1): 39825.
Rehmannioside A是细胞色素P450酶（CYP3A4、2C9和2D6）的抑制剂，IC50值分别为10.08、12.62和16.43μM[1]。Rehmannioside A是一种从Rehmanniae radix分离得到的环烯醚萜苷，具有抗炎、抗氧化、抗凋亡和神经保护等多种生物活性[2, 3]。
在体外，Rehmannioside A（10-300µM）处理小鼠成骨细胞系（MC3T3-E1细胞）24h，在50-200µM时显著提升了暴露于地塞米松的成骨细胞存活率，促进了MC3T3-E1细胞中PI3K/AKT信号通路的激活[4]。Rehmannioside A（20-80µM）处理HK2细胞24h，显著提升了高糖（HG）诱导的HK2细胞的存活率，抑制了细胞凋亡和氧化应激，抑制了细胞内MAPK通路的激活[5]。
在体内，Rehmannioside A（40, 80mg/kg）通过腹腔注射给药治疗血管性痴呆（VD）大鼠14天，剂量依赖性地降低了大鼠海马中TUNEL阳性细胞、活性Caspase-3、PARP和细胞色素c的过度表达[6]。Rehmannioside A（5, 15, 45mg/kg）通过口服治疗5×FAD小鼠，显著改善了小鼠的学习、记忆和认知功能，减少了海马体中Aβ斑块的积累，减少了小胶质细胞数量，增加了PSD 95和突触素-1蛋白表达，减轻了氧化应激和炎症[7]。
| Cell experiment [1]: | |
Cell lines | MC3T3-E1 cells |
Preparation Method | MC3T3-E1 cells were seeded into 96-well plates and treated with Rehmannioside A (10, 25, 50, 100, 150, 200, and 300μM) for 24h. For Dexamethasone treatment, the cells were pretreated with Rehmannioside A for 12h. After 24h of treatment, the cells were washed twice with phosphate-buffered saline and incubated with CCK-8 working solution for 2h at 37°C. The optical density was measured at 450nm using a microplate reader. |
Reaction Conditions | 10, 25, 50, 100, 150, 200, 300μM; 24h |
Applications | Dexamethasone significantly decreased cell viability at 24h, while Rehmannioside A at 50-200μM significantly improved the cell viability of osteoblast exposed to Dexamethasone. |
| Animal experiment [2]: | |
Animal models | Sprague-Dawley (SD) rats |
Preparation Method | Rats were anesthetized using chloral hydrate (350mg/kg, i.p.). Animals were randomly divided into 4 groups (n=20/group): sham-operated rats received the same surgical procedure without the occlusion of double ligation; both carotid arteries were gently separated from the vagus nerve, and permanent artery occlusion was implemented with silk thread. For verification, rats in Vascular dementia (VD) group were randomly subdivided into a control VD Group treated with PBS (VD group), and a 40mg/kg Rehmannioside A(ReA)+VD (ReA-L group) and a 80mg/kg Rehmannioside A+VD (ReA-H group). The sham group consisted of sham-operated rats were treated with PBS (Sham group). RehA was injected intraperitoneally to rats daily for 14 consecutive days. |
Dosage form | 40, 80mg/kg; 14 days; i.p. |
Applications | Vascular dementia (VD) rats exhibited higher percentage of TUNEL and active Caspase-3 positive cells. Rehmannioside A dose-dependently reduced TUNEL and active Caspase-3 expressions. Rehmannioside A could reduce the over-expression of cleaved Caspase-3, PARP, and Cyto-c in the hippocampus of VD rats. |
References: | |
| Cas No. | 81720-05-0 | SDF | |
| 别名 | 地黄甙A | ||
| Canonical SMILES | OCC1(C(C2OC(C(C(O)C3O)O)OC3COC(C(C(O)C4O)O)OC4CO)C(C=CO2)C5O)C5O1 | ||
| 分子式 | C21H32O15 | 分子量 | 524.47 |
| 溶解度 | DMSO: 200 mg/mL (680.7 mM), Need ultrasonic | 储存条件 | Store at -20°C |
| General tips | 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 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.9067 mL | 9.5334 mL | 19.0669 mL |
| 5 mM | 381.3 μL | 1.9067 mL | 3.8134 mL |
| 10 mM | 190.7 μL | 953.3 μL | 1.9067 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >98.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet