product name Sennoside B
Description: Sennoside B is a natural product isolated from Puffer fish, salamanders, frogs foot spot et al., It is a type of irritant laxative that also inhibits PDGF-stimulated cell proliferation. Sennoside B was found to inhibit PDGF-BB-induced phosphorylation of the PDGFR in human MG63 osteosarcoma cells. Pre-incubation of PDGF-BB with sennoside B inhibited the phosphorylation of pathway components including AKT, STAT-5 and ERK1/2.
References: Chem Pharm Bull. 1989;37(10):2744-6; Life Sci. 2009;84(25-26):915-22; Pharmacology. 1988;36 Suppl 1:180-7.
862.74
Formula
C42H38O20
CAS No.
128-57-4
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO:
Water:
Ethanol:
Solubility (In vivo)
Synonyms
other peoduct :
| In Vitro |
In vitro activity: Sennoside B, a kind of irritant laxative isolated from rhei rhizome, inhibits platelet-derived growth factor (PDGF)-stimulated MG63 cell proliferation by binding to PDGF-BB and its receptor and down-regulating the PDGFR-beta signaling pathway. Pre-incubation of PDGF-BB with sennoside B inhibits the phosphorylation of pathway components including Ak strain transforming protein (AKT), signal transducer and activator of transcription 5 (STAT-5) and extracellular signal-regulated kinase 1/2 (ERK1/2). It also inhibits bovine serum monoamine oxidase with IC50 of 9 μM. Kinase Assay: Cell Assay: Human osteosarcoma MG63 cells were treated with PDGF in the presence or absence of sennoside B. Activation of the PDGF signaling pathway was monitored using western immunoblotting with specific antibodies against the PDGF receptor, phosphotyrosine and components of the downstream signaling cascade. Activation of cell metabolism and proliferation was assessed by chromogenic reduction of MTT. |
|---|---|
| In Vivo | Sennosides were tested in a wide range of toxicity studies to evaluate risk assessment. From acute studies, sennosides could be classified as only slightly toxic in rats and mice after a single oral dose. The LD50 values were about 5,000 mg/kg in both species. The cause of death was probably due to an extensive loss of water and electrolytes following massive diarrhoea. In subacute studies with rats (max. 20 mg/kg) and dogs (max. 500 mg/kg), sennosides caused no specific local or systemic toxicity. Minor increase in kidney weight in rats was toxicologically not relevant. In a 6-month study with rats, sennosides were tolerated without specific toxic effects in doses up to 100 mg/kg. Effects on food consumption, body weight gain and some biochemical parameters as well as slight renal lesions can be interpreted as secondary effects following chronic diarrhoea. Mutagenicity tests and reproduction toxicity studies showed no abnormal results. |
| Animal model | Mouse and rat |
| Formulation & Dosage | |
| References | Chem Pharm Bull. 1989 Oct;37(10):2744-6; Life Sci. 2009 Jun 19;84(25-26):915-22; Pharmacology. 1988;36 Suppl 1:180-7. |
