Dihydroisotanshinone I是一种从Salvia trijuga根部分离得到的菲醌衍生物，具有抗氧化作用。
Cas No.:20958-18-3
Sample solution is provided at 25 µL, 10mM.
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Dihydroisotanshinone I is a phenanthrenequinone derivative isolated from the roots of Salvia trijuga, with antioxidant effects [1]. Dihydroisotanshinone I induces ferroptosis in endometrial cancer cells by down-regulating the expression of GPX4, and inhibits the phosphorylation of STAT3 while promoting the reduction of STAT3 protein levels[2]. Dihydroisotanshinone I has been widely used to inhibit the progression of cancer cells, impede the migration ability of cancer cells, and induce DNA damage[3].
In vitro, Dihydroisotanshinone I treatment for 48 hours significantly inhibited the proliferation of A549 cells and H460 cells, with IC50 values of 15.487μM and 19.389μM, respectively[4]. Treatment with 10μM Dihydroisotanshinone I for 48 hours significantly induced apoptosis in HCT 116 cells and decreased the expression of Skp2 protein[5]. Treatment with 5μM Dihydroisotanshinone I for 4 hours significantly induced the expression of Caspase-3 and Caspase-8 in Detroit 562 cells, and increased the phosphorylation levels of ERK1/2, p38 and JNK [6].
In vivo, the 30mg/kg dose of Dihydroisotanshinone I was intraperitoneally injected every two days for 2 weeks, which significantly inhibited the tumor growth in the MCF-7 cell-xenograft mouse models[7]. Intraperitoneal injection of Dihydroisotanshinone I at a dose of 30mg/kg every two days for 18 days significantly inhibited tumor growth in the A549 cell xenograft mouse model without affecting the body weight of the mice[8].
References:
[1] Ip S P, Yang H, Sun H D, et al. Dihydroisotanshinone I protects against menadione-induced toxicity in a primary culture of rat hepatocytes[J]. Planta medica, 2002, 68(12): 1077-1081.
[2] Wu C Y, Yang Y H, Lin Y S, et al. Induction of ferroptosis and apoptosis in endometrial cancer cells by dihydroisotanshinone I[J]. Heliyon, 2023, 9(11).
[3] Lee I Y, Lin Y Y, Yang Y H, et al. Dihydroisotanshinone I combined with radiation inhibits the migration ability of prostate cancer cells through DNA damage and CCL2 pathway[J]. BMC Pharmacology and Toxicology, 2018, 19(1): 5.
[4] Wu C Y, Cherng J Y, Yang Y H, et al. Danshen improves survival of patients with advanced lung cancer and targeting the relationship between macrophages and lung cancer cells[J]. Oncotarget, 2017, 8(53): 90925.
[5] Lin Y Y, Lee I Y, Huang W S, et al. Danshen improves survival of patients with colon cancer and dihydroisotanshinone I inhibit the proliferation of colon cancer cells via apoptosis and skp2 signaling pathway[J]. Journal of Ethnopharmacology, 2017, 209: 305-316.
[6] Hsu C M, Yang M Y, Tsai M S, et al. Dihydroisotanshinone I as a treatment option for head and neck squamous cell carcinomas[J]. International Journal of Molecular Sciences, 2021, 22(16): 8881.
[7] Lin Y S, Shen Y C, Wu C Y, et al. Danshen improves survival of patients with breast cancer and dihydroisotanshinone I induces ferroptosis and apoptosis of breast cancer cells[J]. Frontiers in pharmacology, 2019, 10: 1226.
[8] Wu C Y, Yang Y H, Lin Y S, et al. Dihydroisotanshinone I induced ferroptosis and apoptosis of lung cancer cells[J]. Biomedicine & Pharmacotherapy, 2021, 139: 111585.
Dihydroisotanshinone I是一种从Salvia trijuga根部分离得到的菲醌衍生物，具有抗氧化作用[1]。Dihydroisotanshinone I通过下调GPX4的表达诱导子宫内膜癌细胞发生铁死亡，并抑制STAT3的磷酸化同时促进STAT3蛋白水平的降低[2]。Dihydroisotanshinone I已被广泛用于抑制癌细胞进展、阻碍癌细胞迁移能力并诱导DNA损伤[3]。
在体外，Dihydroisotanshinone I处理48小时显著抑制了A549细胞和H460细胞的增殖，IC50值分别为15.487μM和19.389μM[4]。使用10μM的Dihydroisotanshinone I处理HCT 116细胞48小时，显著诱导细胞凋亡并降低Skp2蛋白的表达[5]。使用5μM的Dihydroisotanshinone I处理Detroit 562细胞4小时，显著诱导Caspase-3和Caspase-8的表达，并增加ERK1/2、p38和JNK的磷酸化水平[6]。
在体内，每两天腹腔注射30mg/kg剂量的Dihydroisotanshinone I，持续2周，显著抑制了MCF-7细胞异种移植小鼠模型中的肿瘤生长[7]。每两天腹腔注射30mg/kg剂量的Dihydroisotanshinone I，持续18天，显著抑制了A549细胞异种移植小鼠模型中的肿瘤生长，且未影响小鼠体重[8]。
| Cell experiment [1]: | |
Cell lines | A549 cells |
Preparation Method | A549 cells were cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS), 1% penicillin-streptomycin at 37℃ in the presence of 5% CO2. A549 cells (1×103) were seeded in each well of a 96-well plate in triplicate. After attachment, the cells were treated with Dihydroisotanshinone I at different concentrations (0, 5, 10, and 20µM) for 48h, then analyzed the cell viability. |
Reaction Conditions | 0, 5, 10, and 20µM; 48h |
Applications | Dihydroisotanshinone I treatment significantly reduced the cell viability of A549 cells in a concentration and time-dependent manner. |
| Animal experiment [2]: | |
Animal models | BALB/c-nu nude mice |
Preparation Method | BALB/c-nu nude mice (18-20g), aged 5-7 weeks, were housed in temperature (23±2°C) and light-controlled (12:12-hour light-dark cycle) animal care facility with food and tap water ad libitum. MCF-7 cells were injected (1×106/Mouse) subcutaneously in the both flanks of nude mice. Mice with tumor sizes of about 10mm3 were selected after about one week. Mice were randomized into two groups and five mice per each group. One group was treated intraperitoneally with vehicle (2.5% DMSO) and the other one group was treated with 30mg/kg Dihydroisotanshinone I every 2 days. Tumor volume and mouse weight were measured every 2-3 days for 2 weeks. Tumor sizes and tumor volume were calculated using the formula length×width×height×0.52. |
Dosage form | 30mg/kg; every 2 days for 2 weeks; i.p. |
Applications | Dihydroisotanshinone I treatment significantly inhibited the tumor growth in the MCF-7 cell-xenograft mouse models. |
References: | |
| Cas No. | 20958-18-3 | SDF | |
| 别名 | 二氢丹参酮 | ||
| Canonical SMILES | O=C1C2=C(C3=C(C=C2)C(C)=CC=C3)C(C4=C1C(C)CO4)=O | ||
| 分子式 | C18H14O3 | 分子量 | 278.3 |
| 溶解度 | DMSO : 6 mg/mL (21.56 mM) | 储存条件 | Store at -20°C |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.5932 mL | 17.9662 mL | 35.9324 mL |
| 5 mM | 718.6 μL | 3.5932 mL | 7.1865 mL |
| 10 mM | 359.3 μL | 1.7966 mL | 3.5932 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
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