中文摘要：

miRNA作为内源性非编码小RNA，主要在转录后水平调控基因表达。近年来越来越多的证据表明，miRNA通过调控脂肪细胞分化相关的转录因子和信号通路来影响脂肪细胞的分化。为探究miR-26a对小鼠（Musmusculus）3T3-L1前脂肪细胞分化的影响及具体的调节作用，本研究分别用miR-26a的agomir和antagomir对miR-26a进行过表达和敲除。结果显示，miR．26a的表达量在3T3-L1细胞分化过程中逐渐上升。过表达miR-26a极显著增加了脂肪合成相关基因——过氧化物酶体增殖物激活受体γ（peroxisome proliferator-activated receptorgamma，纠吼Ry）、脂肪酸合酶（fatty acid synthase，FAS）和脂蛋白脂酶（lipoproteinlipase，LPL）的mRNA水平（P〈0．01），PPARγ和FAS的蛋白水平也显著升高（P〈0．05）。同时，细胞内的脂质聚集也明显增加。相反，抑制miR-26a的表达量降低了3T3．L1细胞的分化。通过靶基因预测和双荧光素酶报告系统分析，证明miR-26a能直接结合到同源性磷酸酶一张力蛋白（phosphataseandtensinhomolog，PTEN）mRNA的3’UTR，并且导致其miRNA和蛋白水平降低（P〈0．05）。本研究的结果表明，miR-26a可能通过直接抑制PTEN来正向的调节3T3-L1细胞的脂肪分化，该结果为miRNA成为治疗肥胖相关疾病的药物靶分子提供了一定的理论依据。

英文摘要：

As an endogenous small non-coding RNA （ncRNA）, microRNAs （miRNAs） regulate gene expression mainly at post-transcriptional level. In recent years, numerous studies have demonstrated that miRNA could have an impact on adipocyte differentiation by modulating the expression of adipogenic transcription factors and signaling molecules. This study showed that the expression of miR-26a gradually rose on day 4 and reached the maximum level on day 8 during 3T3-L1 cell differentiation. In order to investigate the regulatory effects and mechanism of miR-26a on adipogenesis in 3T3-L1 preadipocyte of mouse （Mus musculus）, the miR-26a agomir and antagomir were transfected into 3T3-L1 cells to perform miR26a overexpression and knockdown, respectively. The result showed that miR-26a was significantly overexpressed following agomir transfection on day 2 of differentiation, and the elevated miR-26a expression was maintained until the eighth day after differentiation （P〈0.01）. In contrast, miR-26a was effectively inhibited on day 2, 4 and 8 after induction when the antagomir was transfected into 3T3-L1 cells （P〈0.01）. And overexpression of miR-26a significantly accelerated the relative mRNA expression of genes associated with adipogenesis such as peroxisome proliferator-activated receptor gamma （PPARy）, fatty acid synthase （FAS） and lipoprotein lipase （LPL） （P〈0.01, P〈0.05） on day 2, 4 and 8, and also increased the protein level of PPAR~/and FAS （P〈0.05） on day 8 after differentiation. MiR-26a overexpression also led to a notable increase in lipid accumulation. In contrast, inhibition of miR-26a expression decreased the relative mRNA expression （on day 2, 4 and 8） and the protein level （on day 8） of PPARy and FAS （P〈0.01, P〈0.05） after differentiation. Although there was no significant change in LPL mRNA on day 8 compared to ago-NC group, a significant decrease was detected on day 2 and 4 after differentiation （P〈0.05）. Photomicrograph and quantitative analysis