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MedChemExpressModel (±)-Naringenin - 67604-48-2

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(±)-Naringenin is an orally available anti-inflammatory agent that can regulate both acute and chronic inflammation responses, while also showing antioxidant, neuroprotective, liver-protective, and anti-cancer effects. (±)-Naringenin promotes vasodilation in endothelial cells by activating BKCa channels in muscle cells. It also exerts protective effects against experimental colitis by inhibiting Toll-like receptor 4/NF-κB signaling, making it useful in studies related to sepsis, fulminant hepatitis, fibrosis, and cancer research[1][2][3].
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(±)-Naringenin

MCE China:(±)-Naringenin

Brand:MedChemExpress (MCE)

Cat. No.HY-W011641

CAS:67604-48-2

Purity:98.88%

Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping:Room temperature in continental US; may vary elsewhere.

Description:(±)-Naringenin is an orally available anti-inflammatory agent that can regulate both acute and chronic inflammation responses, while also showing antioxidant, neuroprotective, liver-protective, and anti-cancer effects. (±)-Naringenin promotes vasodilation in endothelial cells by activating BKCa channels in muscle cells. It also exerts protective effects against experimental colitis by inhibiting Toll-like receptor 4/NF-κB signaling, making it useful in studies related to sepsis, fulminant hepatitis, fibrosis, and cancer research.

In Vitro:(±)-Naringenin induces concentration-dependent relaxation in endothelium-denuded aortic rings from rats pre-contracted with 20 mM KCl or norepinephrine, with pIC50 values of 4.74 and 4.68 respectively[1]. (±)-Naringenin increases large conductance calcium-activated potassium (BKCa) current in rat tail artery smooth muscle cells in a concentration-dependent manner[1]. (±)-Naringenin (1-25 μmol/L, 2 h) significantly inhibits TNF-α induced NF-κB luciferase expression in HT29 cells[2]. (±)-Naringenin (25 μmol/L, 2 h) blocks LPS-induced NF-κB p65 nuclear translocation in mouse macrophage RAW264.7 cells[2]. (±)-Naringenin induces apoptosis through both intrinsic (mitochondrial) and extrinsic pathways, upregulating pro-apoptotic genes such as P18, P21, p38, and Bcl-2-associated X protein (Bax), which stimulates mitochondrial cytochrome c release and forms apoptosomes including pro-caspase-9 and apoptosis protease-activating factor 1 (Apaf-1), thereby enhancing caspase-9 expression[3].

In Vivo:(±)-Naringenin (50 mg/kg, orally, once a day for ten days) significantly reduces the severity of DSS-induced colitis in mice and downregulats pro-inflammatory mediators (iNOS, ICAM-1, MCP-1, Cox2, TNF-α, and IL-6 mRNA) in the colonic mucosa[2].

IC50 & Target:NF-κB Caspase 9

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References:

[1]. Saponara S, et al. (+/-)-Naringenin as large conductance Ca(2+)-activated K+ (BKCa) channel opener in vascular smooth muscle cells. Br J Pharmacol. 2006 Dec;149(8):1013-21.  [Content Brief]

[2]. Wei Dou, et al. Protective effect of naringenin against experimental colitis via suppression of Toll-like receptor 4/NF-κB signalling. Br J Nutr. 2013 Aug;110(4):599-608.  [Content Brief]

[3]. Mahzad Motallebi, et al. Naringenin: A potential flavonoid phytochemical for cancer therapy. Life Sci. 2022 Sep 15:305:120752.  [Content Brief]

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