Li Haojing, Li Wenli, Wu Yuanyuan, Wu Huimin, Cai Xiaojun
Heilongjiang Academy of Traditional Chinese Medicine, PR China.
Dazhou Dachuan District People's Hospital, PR China.
Int Immunopharmacol. 2025 Jan 3;145:113719. doi: 10.1016/j.intimp.2024.113719. Epub 2024 Dec 8.
Lotus leaf and its extracts have been reported to exert various beneficial effects; however, their anti-obesity mechanisms remain relatively unclear. Therefore, we investigated the mechanism by which lotus leaf regulates obesity using network pharmacology, molecular docking, and animal experimentation.
Network pharmacology was used to identify potential targets and pathways through which lotus leaf regulates obesity. Molecular docking technology was used to verify the interaction between lotus leaves and core targets of obesity. Additionally, a rat model of obesity induced using a high-fat diet was established to examine the anti-obesity effects of lotus leaf. Moreover, western blotting was performed to examine the expression levels of the target proteins and elucidate the molecular mechanisms of lotus leaf.
Quercetin, nuciferin, catechin, kaempferol, and isorhamnetin were identified as the main active compounds in the lotus leaves involved in obesity treatment. Network pharmacology analysis identified fibroblast growth factor (FGF) 15 and farnesoid X receptor (FXR) as core targets of lotus leaf, and the AGE-RAGE signaling pathway in diabetic complications, neuroactive ligand-receptor interactions, insulin resistance, and cancer pathways, as biomechanistic pathways by which lotus leaf ameliorates obesity. Additionally, molecular docking analysis indicated a strong binding affinity between the main active ingredients of lotus leaf and the core targets. Moreover, western blotting showed that lotus leaf significantly downregulated FGF15 and FXR protein expression in intestinal tissues.
Lotus leaf ameliorates obesity through several pathways, including by downregulating FGF15 and FXR, providing a novel basis for the development of natural drug therapy for obesity.
荷叶及其提取物已被报道具有多种有益作用；然而，其抗肥胖机制仍相对不清楚。因此，我们采用网络药理学、分子对接和动物实验研究了荷叶调节肥胖的机制。
利用网络药理学确定荷叶调节肥胖的潜在靶点和途径。采用分子对接技术验证荷叶与肥胖核心靶点之间的相互作用。此外，建立高脂饮食诱导的大鼠肥胖模型，以研究荷叶的抗肥胖作用。此外，进行蛋白质免疫印迹法检测靶蛋白的表达水平，阐明荷叶的分子机制。
槲皮素、荷叶碱、儿茶素、山奈酚和异鼠李素被确定为荷叶中参与肥胖治疗的主要活性化合物。网络药理学分析确定成纤维细胞生长因子（FGF）15和法尼酯X受体（FXR）为荷叶的核心靶点，糖尿病并发症中的AGE-RAGE信号通路、神经活性配体-受体相互作用、胰岛素抵抗和癌症通路为荷叶改善肥胖的生物力学途径。此外，分子对接分析表明荷叶的主要活性成分与核心靶点之间具有很强的结合亲和力。此外，蛋白质免疫印迹法显示荷叶显著下调肠道组织中FGF15和FXR蛋白的表达。
荷叶通过多种途径改善肥胖，包括下调FGF15和FXR，为开发肥胖天然药物疗法提供了新的依据。
