中文摘要：

采用MTT和流式细胞术分别检测不同浓度的TSA对C3H10T1／2细胞活性和细胞周期分布的影响；油红O染色检测TSA对其成脂分化的影响，实时定量PCR检测TSA对成脂分化的关键转录因子PPAR-γ，以及成脂分化标志物Fabp4和AdipoqmRNA转录的影响．研究去乙酰化酶抑制剂TSA对间充质干细胞C3HIOT1／2增殖和成脂分化的影响及其可能的作用机制．结果显示TSA浓度为1、10和30nmol／L呈浓度依赖性地抑制C3H10T1／2细胞活性，改变细胞形态，并将其细胞周期抑制在G0／G1期；TSA浓度为10nmol／L明显抑制C3H10T1／2细胞的成脂分化作用，并呈浓度依赖性地抑制PPAR-γ、Fabp4和AdipoqmRNA的转录．表明TSA呈剂量依赖性地抑制间充质干细胞C3H10T1／2的增殖和成脂分化，除转录水平调控外，非组蛋白如细胞骨架相关蛋白可能也参与TSA的抑制作用．

英文摘要：

To investigate the effects of histone deaetylase（HDA） inhibitor trichostatin A on proliferation and adipogenie differentiation of C3H10T1/2 mesenehymal stem cells as well as the underlying mechanism. MTT assay and flow cytometry-based cell cycle analysis were used to evaluate the effects of triehostatin （TSA） at different concentrations on cell viability and cell cycle of cultured C3H10T1/2 cells. The influenee of serial concentrations of TSA on adipogenie differentiation of C3H10T1/2 cells was determined by oil red O staining. The effects of TSA on the expression of PPAR-γ, a key adipogenic transcription faetor, and the Fabp4 and Adipoq, the two adipogenie differentiation markers, were determined by realtime PCR. Our results showed that the TSA inhibited the proliferation of C3H10T1/2 cells in a dose-de- pendent manner and the cell cycle of C3H10T1/2 cells was arrested at G0/G1 phase. Moreover, the morphology of C3H10T1/2 cells was found to be flattened by treatment with TSA. The adipogenie differentiation of C3H10T1/2 cells and the expression of PPAR-γ, Fabp4 and Adipoq were suppressed by TSA in a dose-dependent manner. Our study suggested that TSA inhibit the proliferation and adipogenic differentiation of C3H10T1/2 mesenchymal stem cells; in addition to transcriptional regulation, non-histone proteins such as cytoskeleton related proteins, might also be involved in this process.