錦菊素
| 中文名稱 | 錦菊素 |
|---|---|
| 中文同義詞 | 錦菊素;貝萊洛比 |
| 英文名稱 | bigelovin |
| 英文同義詞 | bigelovin;inhibit,Autophagy,Inhibitor,Retinoic acid receptors,Bigelovin,Retinoid X receptors,Apoptosis,Reactive Oxygen Species,RAR/RXR;Azuleno[6,5-b]furan-2,5-dione, 4-(acetyloxy)-3,3a,4,4a,7a,8,9,9a-octahydro-4a,8-dimethyl-3-methylene-, (3aR,4S,4aR,7aR,8R,9aS)- |
| CAS號 | 3668-14-2 |
| 分子式 | C17H20O5 |
| 分子量 | 304.34 |
| EINECS號 | |
| 相關類別 | 標準品-對照品;新品;標準品，對照品 |
| Mol文件 | 3668-14-2.mol |
| 結構式 |  |
錦菊素 性質
| 熔點 | 180-182 °C(Solv: acetone (67-64-1); dichloromethane (75-09-2)) |
|---|---|
| 沸點 | 466.6±45.0 °C(Predicted) |
| 密度 | 1.22±0.1 g/cm3(Predicted) |
| 儲存條件 | 4°C, protect from light |
| 形態(tài) | 固體 |
| 顏色 | 白色至米白色 |
錦菊素提取自旋復花，可用作活性小分子。Bigelovin 是可從海百合中分離得到的一種倍半萜內酯，是選擇性的視黃素 X 受體 α (retinoid X receptor α) 的激動劑。Bigelovin 可通過誘導凋亡和自噬來發(fā)揮抗腫瘤活性。Bigelovin 通過抑制 ROS 的生成來調節(jié) mTOR 信號通路。
Bigelovin (0-20 μM, 24-72 h) significantly inhibits cell viability of liver cancer cells and induces apoptosis and autophagy.
Bigelovin causes a significant increase of p62, LC3B-II, Beclin-1 and a corresponding decrease of p62 levels in a time-dependent manner.
Bigelovin induces cell death involves the suppression of mTOR pathway regulated by ROS production.
Cell Viability Assay
| Cell Line: | HepG2 and SMMC-7721 cells. |
| Concentration: | 0-20 μM. |
| Incubation Time: | 24, 48, 72 h. |
| Result: |
Significantly reduced the cell viability of HepG2 and SMMC-7721 cells in a dose- and time
dependent manner.
No significant difference observed in cell viability of normal liver cell lines, LO2 and LX2, after BigV treatment for 24, 48 or 72 h. |
Western Blot Analysis
| Cell Line: | HepG2 and SMMC-7721 cells. |
| Concentration: | 0-10 μM. |
| Incubation Time: | 24 h. |
| Result: |
The expression of Bcl-2 was decreased, whereas Bax was increased after treatment with BigV. Moreover, Caspase-9, -3 and PARP cleavage were activated significantly after BigV treatment.
|
Bigelovin (BigV, 5, 10, 20 mg/kg) exerts anti-tumor activity in HepG2 xenograft tumor model.
| Animal Model: | HepG2 xenograft model based on the male athymic BALB/c nude mice (5-6 weeks old, 18-22 g). |
| Dosage: | 5, 10, 20 mg/kg. |
| Administration: | Intravenous injection every 2 days. |
| Result: |
The tumor growth rate was significantly slower in BigV treated groups in a dose-dependent manner, along with the reduced tumor weight.
No significant alteration of body weight and hepatic enzyme levels (AST, ALT and LDH) in serum was observed after BigV administration. Western blot findings of tumor tissues indicated the activation of apoptosis and autophagy characterized by the increase of cleaved Caspase-3 and PARP, as well as LC3BII levels. The inactivation of mTOR was also observed in tumor tissues isolated from BigV-treated mice. |