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小叶黑面神上调大鼠脂肪组织和3T3-L1脂肪细胞中过氧化物酶体增殖物激活受体γ的表达。

Labisia pumila Upregulates Peroxisome Proliferator-Activated Receptor Gamma Expression in Rat Adipose Tissues and 3T3-L1 Adipocytes.

作者信息

Mansor Fazliana, Gu Harvest F, Ostenson Claes-Göran, Mannerås-Holm Louise, Stener-Victorin Elisabet, Wan Mohamud Wan Nazaimoon

机构信息

Cardiovascular, Diabetes and Nutrition Research Centre, Institute for Medical Research, 50588 Jalan Pahang, Kuala Lumpur, Malaysia.

出版信息

Adv Pharmacol Sci. 2013;2013:808914. doi: 10.1155/2013/808914. Epub 2013 Jul 7.

Abstract

Peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-activated transcription factor that regulates lipid and glucose metabolism. We investigated the effects of Labisia pumila (LP) standardized water extract on PPARgamma transcriptional activity in adipocytes in vitro and in vivo. We used a rat model of dihydrotestosterone- (DHT-) induced polycystic ovary syndrome (PCOS), a condition characterized by insulin resistance. At 9 weeks of age, the PCOS rats were randomly subdivided into two groups: PCOS-LP (50 mg/kg/day of LP) and PCOS-control (1 mL of deionised water) for 4-5 weeks on the same schedule. Real-time RT-PCR was performed to determine the PPARgamma mRNA levels. LP upregulated PPARgamma mRNA level by 40% in the PCOS rats. Western blot analysis further demonstrated the increased PPARgamma protein levels in parallel with upregulation in mRNA. These observations were further proven by adipocytes culture. Differentiated 3T3-L1 adipocytes were treated with final concentration of 100  μ g/mL LP and compared to untreated control and 10  μ M of rosiglitazone (in type of thiazolidinediones). LP increased PPARgamma expressions at both mRNA and protein levels and enhanced the effect of glucose uptake in the insulin-resistant cells. The data suggest that LP may ameliorate insulin resistance in adipocytes via the upregulation of PPARgamma pathway.

摘要

过氧化物酶体增殖物激活受体γ(PPARγ)是一种配体激活的转录因子,可调节脂质和葡萄糖代谢。我们研究了绒毛润楠(LP)标准化水提取物在体外和体内对脂肪细胞中PPARγ转录活性的影响。我们使用了一种由二氢睾酮(DHT)诱导的多囊卵巢综合征(PCOS)大鼠模型,该疾病以胰岛素抵抗为特征。9周龄时,将PCOS大鼠随机分为两组:PCOS-LP组(每天50mg/kg的LP)和PCOS对照组(1mL去离子水),按相同方案处理4-5周。进行实时RT-PCR以测定PPARγ mRNA水平。LP使PCOS大鼠的PPARγ mRNA水平上调了40%。蛋白质免疫印迹分析进一步证明,PPARγ蛋白水平的增加与mRNA的上调平行。这些观察结果在脂肪细胞培养中得到了进一步证实。用终浓度为100μg/mL的LP处理分化的3T3-L1脂肪细胞,并与未处理的对照组和10μM罗格列酮(噻唑烷二酮类)进行比较。LP在mRNA和蛋白质水平上均增加了PPARγ的表达,并增强了胰岛素抵抗细胞中葡萄糖摄取的效果。数据表明,LP可能通过上调PPARγ途径改善脂肪细胞中的胰岛素抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/572c/3723002/ca2eb04b61e4/APS2013-808914.001.jpg

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