Ying WANG 王穎

我們的研究主要集中在從天然産物及其衍生物中開發小分子抑制劑，旨在調節先天性免疫反應。許多疾病與免疫系統的過度或不足反應有關，因此這一研究領域具有重要意義。我們希望能够通過識別和開發有效的抑制劑，爲此類疾病提供新的治療途徑。

我們特別關注與 Toll 樣受體、炎症小體、泛素化和去泛素化、綫粒體功能及核受體信號轉導相關的信號通路。這些通路在免疫反應的調節中起著關鍵作用，研究它們有助于我們理解和控制各種免疫相關疾病。

目前，我們正著力研究候選抑制劑在控制諸如炎症性腸病、巨噬細胞極化和敗血症等疾病中的適當免疫反應的潜在療效。通過對這些疾病機制的深入研究，我們希望能够發現新的治療策略，改善患者的生活質量。

例如，我們對一系列穿心蓮內酯類似物的結構-活性關係（SAR）進行了詳細分析。這項分析使幫助我們設計、合成了具有更高藥效和特异性的穿心蓮內酯衍生物，經過積極評估這種新化合物在治療炎症性腸病方面的潜力，我們已得到非常令人鼓舞的結果。

此外，我們最近還報道了天然産物衍生物 triptolidiol 可通過調控K63泛素化水平調節 NLRP3 炎症小體活性。基于這一發現，我們正在深入研究炎症小體激活的致病功能，以期揭示其在疾病發展中的獨特作用。

我們竭誠歡迎對分子藥理學感興趣的青年學者加入我們的研究隊伍。詳情請諮詢王穎教授 emilyywang@um.edu.mo.

The primary objective of our research is the development of small molecule inhibitors derived from natural products and their derivatives, with the aim of regulating the innate immune response. This field of study is of great importance, as it has the potential to address a number of diseases that are linked to immune system dysfunction.

Our research is focused on signal transduction pathways associated with Toll-like receptors, inflammasomes, ubiquitination and deubiquitination processes, mitochondrial fitness, and nuclear receptor signaling. These pathways play a pivotal role in immune regulation, and a deeper comprehension of them may pave the way for groundbreaking treatments for immune-related conditions. At present, our research is focused on the potential therapeutic efficacy of these inhibitor candidates in the management of diseases such as inflammatory bowel disease, macrophage polarization, and sepsis. The objective is to identify novel therapeutic strategies by elucidating the mechanisms through which these inhibitors modulate the immune response in these conditions.

For example, a detailed structure-activity relationship (SAR) analysis was conducted on a series of andrographolide analogs. This analysis informed the synthesis of a novel andrographolide analog, which is currently being evaluated for its potential therapeutic efficacy in the treatment of inflammatory bowel disease. The initial findings are encouraging, indicating substantial therapeutic potential. Furthermore, we recently identified the natural product derivative triptolidiol, which directly modifies the K63-linked ubiquitination of NLRP3 and modulates inflammasome assembly. We are currently conducting more comprehensive investigations into the pathogenic functions of inflammasome activation, with the aim of enhancing our understanding of its role in disease progression.

Through these endeavours, we aspire to advance scientific knowledge and provide novel, efficacious treatment options for clinical use.

We are actively looking for young talents interested in our molecular pharmacology research projects. For more information, please contact Prof. Wang at emilyywang@um.edu.mo.