包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
5mg | 电议 |
10mg | 电议 |
25mg | 电议 |
50mg | 电议 |
100mg | 电议 |
Cell experiment: | Forsythoside B is dissolved in sterile saline solution and added to the medium at various concentrations (from 0.1 to 10 μM) and incubated with LPS stimulated RAW264.7 cells. Cell-free supernatants are collected after Forsythoside B treatment for 24 h. Cell viability is assessed by measuring lactate dehydrogenase (LDH) in the medium[1]. |
Animal experiment: | Rats: Forsythoside B is dissolved in sterilized saline. For the dose–response study, forsythoside B at doses of 1.3, 3.2, 8, 20 or 50 mg/kg is administered as an intravenous bolus injection at 15 min after reperfusion. The sham or vehicle-treated rats are injected with saline. Neurological deficits are determined at 23 h after reperfusion followed by brain infarct volume examination[2]. |
产品描述 | Forsythoside B is a phenylethanoid glycoside isolated from the leaves of Lamiophlomis rotata Kudo, a Chinese folk medicinal plant for treating inflammatory diseases and promoting blood circulation. Forsythoside B could inhibit TNF-alpha, IL-6, IκB and modulate NF-κB. Forsythoside B concentration-dependently down-regulates the levels of TNF-α, IL-6 and high-mobility group-box 1 protein (HMGB1) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells, inhibits the IκB kinase (IKK) pathway and modulated nuclear factor (NF)- κB[1]. Intravenous injection of forsythoside B alone or plus imipenem reduces serum levels of TNF-α, IL-6, HMGB1, triggering receptor expressed on myeloid cells (TREM-1) and endotoxin, while the serum level of IL-10 is up-regulated and myeloperoxidase (MPO) in lung, liver and small intestine is reduced[1]. Forsythoside B at doses higher than 8 mg/kg produces a significant neuroprotective potential in cerebral ischemia and reperfusion rats. Forsythoside B (20 mg/kg) demonstrates significant neuroprotective activity even after delayed administration at 1 h, 3 h and 5 h after cerebral ischemia and reperfusion. Forsythoside B 20 mg/kg attenuates histopathological damage as demonstrated by smaller brain infarct size and brain edema, decreased cerebral Evans blue extravasation and myeloperoxidase activity, inhibited cerebral phosphor-IκB-α and NF-κB expression[2]. Forsythoside B shows a significant recovery in myocardial function with improvement of LVSP and +/-dp/dt(max). The myocardial infarct volume, serum levels of Tn-T, TNF-alpha and IL-6, content of MDA and MPO activity in myocardial tissue are all reduced, protein expression of HMGB1, phosphor-I kappaB-alpha and phosphor-NF-kappaB are down-regulated, while attenuate the decrease of SOD and GPx activities[3]. References: |