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Naringenin

CAS No. : 480-41-1

MCE 站：Naringenin

产品活性：Naringenin是葡萄柚中主要的黄烷酮; 显示出强烈的抗炎和抗氧化活性。Naringenin 具有抗登革热病毒 (DENV) 活性。

研究领域：Cell Cycle/DNA Damage  |  Metabolic Enzyme/Protease  |  Immunology/Inflammation  |  NF-κB  |  Anti-infection

作用靶点：PPAR  |  Reactive Oxygen Species  |  Influenza Virus  |  Endogenous Metabolite

In Vitro: 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.

In Vivo: 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.

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