CAS NO: | 102040-03-9 |
包装: | 20mg |
市场价: | 431元 |
Cas No. | 102040-03-9 |
别名 | 土贝母苷甲; Tubeimoside-1; Lobatoside-H |
化学名 | Tubeimoside I |
Canonical SMILES | C[C@@]1([H])[C@@](O)([H])[C@](O[C@@]2([H])[C@@](O)([H])[C@](O)([H])[C@@](O)([H])CO2)([H])[C@](O)([H])[C@@](O[C@]3([H])[C@](O)([H])[C@](O)([H])CO[C@@]3([H])OC([C@]4(CC[C@]56C)CCC(C)(C[C@@]4([H])C5=CC[C@]7([H])[C@@](C[C@@](O)([H])[C@@](O8)([H])[C@]9(COC(C[C |
分子式 | C63H98O29 |
分子量 | 1319.43 |
溶解度 | ≥ 131.9mg/mL in Water |
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while. |
Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
产品描述 | Tubeimoside I(Lobatoside-H) is an extract from Chinese herbal medicine Bolbostemma paniculatum (MAXIM.) FRANQUET (Cucurbitaceae) has been shown as a potent anti-tumor agent for a variety of human cancers.IC50 value:Target: Anticancer natural compoundin vitro: TBMS I inhibited the proliferation of both HepG2 and L-02 cells in a dose- and time-dependent manner, but HepG2 cells appeared more sensitive to the agent. When exposed to TBMS I for 24, 48 and 72 h, IC50 for HepG2 cells versus L-02 cells were 15.5 vs. 23.1, 11.7 vs. 16.2, 9.2 vs. 13.1 (μM, p<0.01), respectively. TBMS I induced cell shrinkage, nuclear condensation and fragmentation, cell cycle arrest at the G2/M phase, mitochondrial membrane disruption, release of cytochrome c from the mitochondria, activation of caspase 3 and 9, and shifting Bax/Bcl-2 ratio from being anti-apoptotic to pro-apoptotic, all indicative of initiation and progression of apoptosis involving mitochondrial dysfunction [1]. TBMS1-induced molecular events were related to mitochondria-induced intrinsic apoptosis and P21-cyclin B1/cdc2 complex-related G2/M cell cycle arrest [2]. TBMS1 combined with CDDP promoted cell apoptosis, decreased proliferation activity and increased cytosolic Ca2+ levels. Bcl-2 protein expression was down-regulated but Bax was up-regulated. Moreover, GST-π mRNA and protein expression were decreased. TBMS1 reduced the resistance of the cells to CDDP-induced cytotoxicity [4]. Treatment with TBMS1 resulted in dose- and time-dependent inhibition of proliferation, led to arrest in phase G2/M of the cell cycle and increased the levels of intracellular Ca2 . Furthermore, TBMS1 up-regulated the levels of the glucose-regulated protein 78/immunoglobuin heavy chain binding protein (GRP78/Bip), C/EBP homologous protein (CHOP), Bax, and cleaved caspase-3 and down-regulated the levels of Bcl-2 [5].in vivo: TBMS1 significantly inhibited the production of the pro-inflammatory cytokines, TNF-α, IL-6 and IL-1β in vitro and in vivo. Pretreatment with TBMS1 markedly attenuated the development of pulmonary edema, histological severities and inflammatory cells infiltration in mice with ALI [3]. References: |