胰岛素抵抗（Insulin Resistance，IR）是多种代谢疾病重要的病理改变，也是近年来中药防治代谢疾病研究的热点。PPARγ是调控脂肪分化的关键转录因子，脂肪分化可增强脂肪细胞对脂质的贮存能力，改善IR。我们研究发现：黄连花薹提取物中富含蒙花苷，且蒙花苷可改善高脂喂养导致的小鼠IR，促进3T3-L1前脂肪细胞分化，上调PPARγ及下游基因表达，但具体机制尚不清楚。据此提出假说：蒙花苷可能通过调控PPARγ介导的脂肪分化改善IR。本研究拟从细胞和整体水平，全面系统地评价蒙花苷对IR的作用；在作用机制方面，基于PPARγ介导的脂肪分化，结合RNA干扰、报告基因、分子对接、生物素标记小分子探针等技术，深入探讨蒙花苷改善IR的作用机制。项目预期可阐明蒙花苷通过PPARγ介导的脂肪分化改善IR的作用及机制，以期为蒙花苷及黄连花薹的合理利用提供理论基础，也为IR相关代谢疾病的防治提供新思路。

Insulin Resistance (IR) is an important pathological change in many metabolic diseases, and is also a hotspot in the research on the prevention and treatment of metabolic diseases with traditional Chinese medicine in recent years. PPARγ is a key transcription factor in the regulation of adipogenesis, which can enhance the lipid storage capacity of adipocytes and improve IR. In our preliminary study, Coptis chinensis inflorescence extract was rich in linarin, which could improve the high-fat diet induced IR in mice. Linarin could also promote the differentiation of 3T3-L1 pre-adipocytes, and up-regulate the expression of PPARγ and its downstream genes, but the specific mechanism was still unclear. Based on these results, a scientific hypothesis was proposed that linarin might improve IR by regulating PPARγ mediated adipogenesis. The purpose of this study is to evaluate the effect of linarin on IR comprehensively and systematically at both cell and animal levels. The molecular mechanism of linarin to improve IR was further explored based on PPARγ mediated adipogenesis, combined with RNA interference, dual-luciferase report gene system, molecular docking, biotin-labeled small molecule probe and other technologies. The study is expected to elucidate the effect and mechanism of linarin in improving IR through PPARγ mediated adipogenesis, so as to provide a theoretical basis for the rational utilization of linarin and C. chinensis inflorescence, and provide new ideas for the treatment of IR related metabolic diseases.