Naringenin

Research use only, not for human use.

Naringenin is a flavanone that is considered to have a bioactive effect on human health as antioxidant, free radical scavenger, antiinflammatory, carbohydrate metabolism promoter, immunity system modulater. This substance has also been shown to repair DNA.

Naringenin is a bioflavonoid drug potentially for the treatment of HCV infection. has antioxidant and chelating effects in the liver. Naringenin significantly suppressed UVB-induced extracellular signal-regulated kinase 2 (ERK2) activity and subsequently attenuated UVB-induced phosphorylation of p90(RSK) by competitively binding with ATP. Naringenin exerts potent anti-photoaging effects by suppressing ERK2 activity and decreasing FRA1 stability, followed by down-regulation of AP-1 transactivation and MMP-1 expression. Naringenin blocks TGF-β1 trafficking from the trans-Golgi network by suppressing PKC activity, resulting in a reduction of TGF-β1 secretion from breast cancer cells.

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. 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.

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. 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. 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.

Naringenin | NSC 11855 | NSC-11855 | NSC11855

Others

Other Targets

CYP1A2

Inflammation/Immunology

——

480-41-1

272.26

C15H12O5

>98% (HPLC)

DMSO : ≥ 50 mg/mL; 183.65 mM

C1[C@H](Oc2cc(cc(c2C1=O)O)O)c1ccc(cc1)O

(S)-5,7-dihydroxy-2-(4-hydroxyphenyl)chroman-4-one

(-20℃)

With Ice Pack

≥ 2 years