Naringenin 

Naringenin is the predominant flavanone in Citrus reticulata Blanco; displays strong anti-inflammatory and antioxidant activities. Naringenin has anti-dengue virus (DENV) activity.

Naringenin is shown to inhibit the proliferation of HepG2 cells resulted partly from an accumulation of cells in the G0/G1 and G2/M phase of the cell cycle. Naringenin has been shown to induce apoptosis as evidenced by nuclei damage and increased proportion of apoptotic cells. Naringenin triggers the mitochondrial-mediated apoptosis pathway as shown by an increased ratio of Bax/Bcl-2, subsequent release of cytochrome C, and sequential activation of caspase-3^[1]. Naringenin exposure significantly reduces the cell viability of A431 cells with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. Cell cycle study shows that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis reveal a dose dependent increment in caspase-3 activity which leads to cell apoptosis^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Naringenin supplementation causes a significant reduction in the amount of total triglyceride and cholesterol in plasma and liver. In addition, naringenin supplementation lowers adiposity and triglyceride contents in parametrial adipose tissue. Naringenin-fed animals show a significant increase in PPARα protein expression in the liver. The expression of CPT-1 and UCP2, known to be regulated by PPARα, is markedly enhanced by naringenin treatment^[3]. Naringenin increases hepatic fatty acid oxidation through a PPARγ coactivator 1α/PPARα-mediated transcription program. It prevents sterol regulatory element-binding protein 1c–mediated lipogenesis in both liver and muscle by reducing fasting hyperinsulinemia. Naringenin decreases hepatic cholesterol and cholesterol ester synthesis^[4]. Naringenin inhibits TNF-α-induced VSMC proliferation and migration in a dose-dependent manner. Mechanistic study demonstrates that naringenin prevents ERK/MAPK and Akt phosphorylation while left p38 MAPK and JNK unchanged. Naringenin also blocks the increase of ROS generation induced by TNF-α^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

272.25

C₁₅H₁₂O₅

480-41-1

Solid

White to light yellow

O=C1C[C@@H](C2=CC=C(O)C=C2)OC3=CC(O)=CC(O)=C13

Room temperature in continental US; may vary elsewhere.

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

• [1]. Arul D, et al. Naringenin (citrus flavonone) induces growth inhibition, cell cycle arrest and apoptosis in human hepatocellular carcinoma cells. Pathol Oncol Res. 2013 Oct;19(4):763-70.  [Content Brief]

  [2]. Ahamad MS, et al. Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinomacell through ROS generation and cell cycle arrest. PLoS One. 2014 Oct 16;9(10):e110003.  [Content Brief]

  [3]. Cho KW, et al. Dietary naringenin increases hepatic peroxisome proliferators-activated receptor α proteinexpression and decreases plasma triglyceride and adiposity in rats. Eur J Nutr. 2011 Mar;50(2):81-8.  [Content Brief]

  [4]. Mulvihill EE, et al. Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDLreceptor-null mice with diet-induced insulin resistance. Diabetes. 2009 Oct;58(10):2198-210.  [Content Brief]

  [5]. Chen S, et al. Naringenin inhibits TNF-α induced VSMC proliferation and migration via induction of HO-1. Food Chem Toxicol. 2012 Sep;50(9):3025-31.  [Content Brief]

  [6]. Frabasile S, et al. The citrus flavanone naringenin impairs dengue virus replication in human cells. Sci Rep. 2017 Feb 3;7:41864.  [Content Brief]