Ahn Jiyun, Lee Hyunjung, Kim Suna, Park Jaeho, Ha Taeyoul
Food Function Research Center, Korea Food Research Institute, 516, Baekhyun-dong, Bundang-gu, Seongnam-si, Gyeonggi-do 463-746, Republic of Korea.
Biochem Biophys Res Commun. 2008 Sep 5;373(4):545-9. doi: 10.1016/j.bbrc.2008.06.077. Epub 2008 Jun 27.
Quercetin is the most abundant flavonoid and is assumed to have protective roles against the pathogenesis of multiple diseases associated with oxidative stress. In the present study, we investigated the molecular mechanisms by which quercetin affects adipogenesis and apoptosis in 3T3-L1 cells. The exposure of 3T3-L1 preadipocytes to quercetin resulted in attenuated adipogenesis and decreased expression of adipogenesis-related factors and enzymes. Moreover, quercetin exposure up-regulated the levels of phosphorylated adenosine monophosphate-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase (ACC). Treatment of 3T3-L1 adipocytes with quercetin resulted in the induction of apoptosis and a concomitant decrease in ERK and JNK phosphorylation. Taken together, these data indicate that quercetin exerts anti-adipogenesis activity by activating the AMPK signal pathway in 3T3-L1 preadipocytes, while the quercetin-induced apoptosis of mature adipocytes was mediated by modulation of the ERK and JNK pathways, which play pivotal roles during apoptosis.
槲皮素是最丰富的黄酮类化合物，被认为对多种与氧化应激相关疾病的发病机制具有保护作用。在本研究中，我们探究了槲皮素影响3T3-L1细胞脂肪生成和凋亡的分子机制。将3T3-L1前脂肪细胞暴露于槲皮素会导致脂肪生成减弱以及脂肪生成相关因子和酶的表达降低。此外，槲皮素暴露上调了磷酸化的腺苷单磷酸激活蛋白激酶（AMPK）及其底物乙酰辅酶A羧化酶（ACC）的水平。用槲皮素处理3T3-L1脂肪细胞会导致细胞凋亡诱导以及ERK和JNK磷酸化同时降低。综上所述，这些数据表明槲皮素通过激活3T3-L1前脂肪细胞中的AMPK信号通路发挥抗脂肪生成活性，而槲皮素诱导的成熟脂肪细胞凋亡是由ERK和JNK通路的调节介导的，这两条通路在凋亡过程中起关键作用。
