Kim Jin-Kyung, So Hongseob, Youn Myung-Ja, Kim Hyung-Jin, Kim Yunha, Park Channy, Kim Se-Jin, Ha Young-Ae, Chai Kyu-Yun, Kim Shin-Moo, Kim Ki-Young, Park Raekil
Vestibulocochlear System Research Center & Department of Microbiology, Wonkwang University School of Medicine, Iksan, Jeonbuk 570-749, Republic of Korea.
J Ethnopharmacol. 2007 Nov 1;114(2):260-7. doi: 10.1016/j.jep.2007.08.028. Epub 2007 Aug 19.
Hibiscus sabdariffa L., a tropical beverage material and medical herb, is used commonly as in folk medicines against hypertension, pyrexia, inflammation, liver disorders, and obesity. This report was designed to investigate the inhibitory mechanisms of hibiscus extract on adipocyte differentiation in 3T3-L1 preadipocytes. The possible inhibitory pathways that regulate the adipocyte differentiation contain the adipogenic transcription factors, C/EBPalpha and PPARgamma, PI3-kinase, and MAPK pathway. In this study, we examined whether hibiscus extract affected the adipogenesis via these three pathways. To differentiate preadipocyte in adipocyte, confluent 3T3-L1 preadipocytes were treated with the hormone mixture including isobutylmethylxanthine, dexamethasone, and insulin (MDI). Hibiscus extract inhibited significantly the lipid droplet accumulation by MDI in a dose-dependent manner and attenuated dramatically the protein and mRNA expressions of adipogenic transcriptional factors, C/EBPalpha and PPARgamma, during adipogenesis. The increase of phosphorylation and expression of PI3-K/Akt during adipocytic differentiation was markedly inhibited by treatment with hibiscus extract or PI3-K inhibitors. Furthermore, the phosphorylation and expression of MEK-1/ERK known to regulate the early phase of adipogenesis were clearly decreased with the addition of hibiscus extract. Taken together, this report suggests that hibiscus extract inhibits the adipocyte differentiation through the modulation of PI3-K/Akt and ERK pathway that play pivotal roles during adipogenesis.
玫瑰茄,一种热带饮料原料和药草,在民间医学中常用于治疗高血压、发热、炎症、肝脏疾病和肥胖症。本报告旨在研究玫瑰茄提取物对3T3-L1前脂肪细胞脂肪生成的抑制机制。调节脂肪生成的可能抑制途径包括脂肪生成转录因子C/EBPα和PPARγ、PI3激酶和MAPK途径。在本研究中,我们研究了玫瑰茄提取物是否通过这三种途径影响脂肪生成。为了将前脂肪细胞分化为脂肪细胞,用包含异丁基甲基黄嘌呤、地塞米松和胰岛素(MDI)的激素混合物处理汇合的3T3-L1前脂肪细胞。玫瑰茄提取物以剂量依赖的方式显著抑制MDI诱导的脂滴积累,并在脂肪生成过程中显著减弱脂肪生成转录因子C/EBPα和PPARγ的蛋白质和mRNA表达。用玫瑰茄提取物或PI3-K抑制剂处理可显著抑制脂肪细胞分化过程中PI3-K/Akt磷酸化和表达的增加。此外,添加玫瑰茄提取物后,已知调节脂肪生成早期阶段的MEK-1/ERK的磷酸化和表达明显降低。综上所述,本报告表明玫瑰茄提取物通过调节在脂肪生成过程中起关键作用的PI3-K/Akt和ERK途径来抑制脂肪细胞分化。