产品
编 号：F337907
分子式：C17H20O5
分子量：304.34
分子式：C17H20O5
分子量：304.34
产品类型
规格
价格
是否有货
5mg
询价
询价
10mg
询价
询价
结构图
CAS No: 3668-14-2
产品详情
生物活性：
Bigelovin, a sesquiterpene lactone isolated from Inula hupehensis, is a selective retinoid X receptor α agonist. Bigelovin suppresses tumor growth through inducing apoptosis and autophagy via the inhibition of mTOR pathway regulated by ROS generation.
体内研究：
Bigelovin (BigV，5，10，20 mg/kg) 在 HepG2 异种移植肿瘤模型中发挥抗肿瘤活性。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 LC3BIIlevels. The inactivation of mTOR was also observed in tumor tissuesisolated from BigV-treated mice.
体外研究：
Bigelovin (0 -20 μM，24-72 h) 显著抑制肝癌细胞的细胞活力并诱导细胞凋亡和自噬。 Bigelovin 显著增加p62、LC3B-II，Beclin-1 和 p62 水平的相应降低呈时间依赖性。Bigelovin 诱导细胞死亡涉及抑制由 ROS 产生调节的 mTOR 通路。
Bigelovin, a sesquiterpene lactone isolated from Inula hupehensis, is a selective retinoid X receptor α agonist. Bigelovin suppresses tumor growth through inducing apoptosis and autophagy via the inhibition of mTOR pathway regulated by ROS generation.
体内研究：
Bigelovin (BigV，5，10，20 mg/kg) 在 HepG2 异种移植肿瘤模型中发挥抗肿瘤活性。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 LC3BIIlevels. The inactivation of mTOR was also observed in tumor tissuesisolated from BigV-treated mice.
体外研究：
Bigelovin (0 -20 μM，24-72 h) 显著抑制肝癌细胞的细胞活力并诱导细胞凋亡和自噬。 Bigelovin 显著增加p62、LC3B-II，Beclin-1 和 p62 水平的相应降低呈时间依赖性。Bigelovin 诱导细胞死亡涉及抑制由 ROS 产生调节的 mTOR 通路。
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