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Polyinosinic-polycytidylic acid _ MedChemExpress (MCE)

閱讀:163      發(fā)布時(shí)間:2024-3-1
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Polyinosinic-polycytidylic acid

MCE 國(guó)際站:Polyinosinic-polycytidylic acid

CAS:24939-03-5

品牌:MedChemExpress (MCE)

存儲(chǔ)條件:Powder: -20°C, 3 years.In solvent: -80°C, 6 months; -20°C, 1 month.

生物活性:聚肌胞苷酸 (Poly(I:C)) 是一種合成的雙鏈 RNA (dsRNA),是一種 Toll 樣受體 3 (TLR3) 激動(dòng)劑。聚肌胞苷酸存在于某些病毒中,因此通常用于模擬細(xì)胞外 dsRNA 的作用。

體外:Polyinosinic-polycytidylic acid (0.5-5 μg/mL, 3-24 h) 呈現(xiàn)劑量和時(shí)間依賴性增加誘導(dǎo)永生化氣道上皮細(xì)胞的細(xì)胞旁通透性[4]。 Polyinosinic-polycytidylic acid (5 μg/mL, 24 h) 對(duì) 16HBE14o- 細(xì)胞沒(méi)有細(xì)胞毒性[4]。 Polyinosinic-polycytidylic acid (5 μg/mL, 6 h) 在 16HBE14o- 細(xì)胞中誘導(dǎo)上皮頂端連接復(fù)合體和緊密連接的破壞[4]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only.

體內(nèi):Polyinosinic-polycytidylic acid (2.5-10 mg/mL, Stereotaxic injection, single dose) 在腦黑質(zhì)和背外側(cè)紋狀體中誘導(dǎo)持續(xù)的炎癥反應(yīng)[2]。 Polyinosinic-polycytidylic acid (10 μg/mouse, Intraperitoneal injection, single dose) 降低小鼠的肺腫瘤生長(zhǎng)[3]。 Polyinosinic-polycytidylic acid (1.25 mg/kg, Intraperitoneal injection, single dose) 在 MCAO 模型小鼠中通過(guò) TLR3 下調(diào)TLR4/MyD88 信號(hào)通路發(fā)揮腦缺血再灌注損傷的治療作用[5]。 MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: lung tumor-bearing mice[3] Dosage: 10 μg/mouse Administration: Intraperitoneal injection (i.p.) Result: Induced a significant decrease in the growth of pulmonary metastases in tumor-bearing mice. Reduced the amount of lung foci to ≈ 40%. Significantly increased BAL fluid cell numbers. Increased the level of INF-γ and IL-17A, decreased the levels of IL-13. Increased TLR3 expression. Animal Model: Middle cerebral artery occlusion (MCAO) model mice[5] Dosage: 1.25 mg/kg Administration: Intraperitoneal injection (i.p.) Result: Reduced focal cerebral I/R injury. Increased the expression of Bcl2, Hsp27, and Hsp70, decreased Bax expression, and reduced cellular degeneration and apoptosis. Protected against cerebral ischemia and conferred protection against cerebral I/R injury through the downregulation of TLR4 signaling via TLR3.

銷售產(chǎn)品:Ginsenoside Rh2  | PMSF  | GW3965 (hydrochloride)  | Sodium 4-phenylbutyrate  | 2-Hydroxy Atorvastatin-d5 (disodium)  | Erlotinib  | Elinzanetant  | TBHQ  | GSK2795039  | Relatlimab

研究領(lǐng)域:Immunology/Inflammation  |  Apoptosis  |  Cell Cycle/DNA Damage  |  Metabolic Enzyme/Protease

作用靶點(diǎn):Toll-like Receptor (TLR)  |  PKD  |  HSP  |  Bcl-2 Family  |  Interleukin Related

Trending products:Recombinant Proteins  |  Bioactive Screening Libraries  |  Natural Products  |  Fluorescent Dye  |  PROTAC  |  Isotope-Labeled Compounds  |  Oligonucleotides

參考文獻(xiàn):

[1]. Alexopoulou L, Holt AC, Medzhitov R, Flavell RA. Recognition of double-stranded RNA and activation of NF-kappaB by Toll-like receptor 3. Nature. 2001;413(6857):732-738.

[2]. Matsumoto M, Kikkawa S, Kohase M, Miyake K, Seya T. Establishment of a monoclonal antibody against human Toll-like receptor 3 that blocks double-stranded RNA-mediated signaling. Biochem Biophys Res Commun. 2002;293(5):1364-1369.

[3]. Cheng Y, Xu F. Anticancer function of polyinosinic-polycytidylic acid [J]. Cancer biology & therapy, 2010, 10(12): 1219-1223.

[4]. Deleidi M, Hallett P J, Koprich J B, et al. The Toll-like receptor-3 agonist polyinosinic: polycytidylic acid triggers nigrostriatal dopaminergic degeneration [J]. Journal of Neuroscience, 2010, 30(48): 16091-16101.

[5]. Forte G, Rega A, Morello S, et al. Polyinosinic-polycytidylic acid limits tumor outgrowth in a mouse model of metastatic lung cancer [J]. The Journal of Immunology, 2012, 188(11): 5357-5364.

[6]. Rezaee F, Meednu N, Emo J A, et al. Polyinosinic: polycytidylic acid induces protein kinase D–dependent disassembly of apical junctions and barrier dysfunction in airway epithelial cells [J]. Journal of Allergy and Clinical Immunology, 2011, 128(6): 1216-1224. e11.

[7]. Wang P F, Fang H, Chen J, et al. Polyinosinic-polycytidylic acid has therapeutic effects against cerebral ischemia/reperfusion injury through the downregulation of TLR4 signaling via TLR3 [J]. The Journal of Immunology, 2014, 192(10): 4783-4794.

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