| 包装 | 价格(元) |
| 10mM (in 1mL Water) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | BEAS-2B cells |
Preparation Method | BEAS-2B cells were seeded in 6-well plates one day before Poly (I:C) treatment. One hour before infection at multiplicity of infection (MOI) 0.01, 1, or 5, the cells were pre-treated with 4 μg/ml of Poly (I:C) or left untreated. After adsorption, the cells were maintained in the medium with or without Poly (I: C) (4 μg/ml). The CPE was observed at 24, 48, and 72 h postinfection (p.i.) under a microscope. |
Reaction Conditions | 4 μg/ml Poly (I: C) for 24/48/72 h |
Applications | Poly (I:C) suppressed cytopathic effects (CPE) induced by CHIKV infection in BEAS-2B cells in the presence of Poly (I:C) and inhibited the replication of CHIKV in the cells. The virus titers of Poly (I:C)-treated cells were much lower compared with those of untreated cells. CHIKV infection and Poly (I:C) treatment of BEAS-2B cells induced the production of IFN-β and increased the expression of anti-viral genes, including IFN-α, IFN-β, MxA, and OAS. Both Poly (I:C) and CHIKV infection upregulate the expression of TLR3 in BEAS-2B cells. |
Animal models | C57BL/6J mouse |
Preparation Method | Injection of MC38 cells into C57BL/6J mice and the subsequent intraperitoneal injections of Poly(I:C),Mice were treated with 50 μg Poly(I:C) by intraperitoneal injection on days 8, 11, 14, 17, 20 and 23. |
Dosage form | 50 μg Poly(I:C) by intraperitoneal injection on days 8, 11, 14, 17, 20 and 23. |
Applications | Poly(I:C)-activated macrophages displayed enhanced phagocytosis after CD47 blockade. Compared with mice receiving monotherapy, those received Poly(I:C) in combination with anti-CD47 mAb exhibited significantly inhibited tumor growth. Moreover, in vivo delivery of Poly(I:C) plus anti-CD47 mAb to tumor-bearing mice altered the tumor immune microenvironment. |
| 产品描述 | Poly (I:C), a synthetic double-stranded RNA (dsRNA) analog, is an immunostimulant that acts as the most potent interferon (IFN) inducer. Toll-like receptor- 3 (TLR3) agonist[1]. Poly (I:C) suppressed cytopathic effects (CPE) induced by CHIKV infection in BEAS-2B cells in the presence of Poly (I:C) and inhibited the replication of CHIKV in the cells. Both Poly (I:C) and CHIKV infection upregulate the expression of TLR3 in BEAS-2B cells[1].DsRNA poly(I:C) up-regulated the expression of IFNβ and apoptosis-associated genes in cervical cancer cells, activating both intrinsic and extrinsic apoptotic pathways, and eventually inducing cell death[8].Stable maturation of DC can be simply induced by the addition of polyriboinosinic polyribocytidylic acid (poly(I:C))[3].Poly(I:C) decreased the rate of successful in vitro fertilization via DNA damage and abnormal spindle morphology at the first cleavage and inhibited early embryonic development by inducing immune response and promoting blastocyst cell apoptosis[9]. Mixtures that included the TLR7/8 agonists R848 or CL075, combined with the Poly (I:C), yield 3-d mature dendritic cells[2]. Poly(I:C)-activated macrophages displayed enhanced phagocytosis after CD47 blockade. Compared with mice receiving monotherapy, those received Poly(I:C) in combination with anti-CD47 mAb exhibited significantly inhibited tumor growth[4]. In vivo, poly(I:C) enhanced cell surface expression of Mac-1 on neutrophils in mice and facilitated their infiltration to lung tissues. Poly(I:C) also downregulated thrombomodulin expression in mouse tissues and reduced its circulating soluble level in plasma[5].1.25 and 5 mg/kg poly(I:C) preconditioning significantly reduced myocardial infarct size and cardiac dysfunction. Moreover, poly(I:C) significantly promoted cell survival by restoring autophagy flux and then regulating it to an adequate level Increased autophagy protein Beclin1 and LC3II together with p62 degradation after additional chloroquine[6].In mice,following Poly I:C exposure, a significant decrease in DA-D2 receptor binding, reduction in corpus callosum calibre and MOG immunolabelling indicating demyelination and a significant decrease in locomotor activity, neuromuscular strength and motor coordination signify motor deficits and hypokinetic influence of early life viral infection[7]. References: |
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