Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Rehabilitation Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Phytomedicine. 2024 Feb;124:155268. doi: 10.1016/j.phymed.2023.155268. Epub 2023 Dec 7.
Obesity has emerged as a global epidemic. Recent research has indicated that diet-induced obesity can be prevented by promoting lacteal junction zippering. Berberine, which is derived from natural plants, is found to be promising in weight reduction, but the underlying mechanism remains unspecified.
To determine whether berberine protects against obesity by regulating the lacteal junction and to explore potential molecular mechanisms.
Following the induction of the diet-induced obese (DIO) model, mice were administered low and high doses of berberine for 4 weeks. Indicators associated with insulin resistance and lipid metabolism were examined. Various methods, such as Oil Red O staining, transmission electron microscopy imaging, confocal imaging and others were used to observe the effects of berberine on lipid absorption and the lacteal junction. In vitro, human dermal lymphatic endothelial cells (HDLECs) were used to investigate the effect of berberine on LEC junctions. Western Blot and immunostaining were applied to determine the expression levels of relevant molecules.
Both low and high doses of berberine reduced body weight in DIO mice without appetite suppression and ameliorated glucolipid metabolism disorders. We also found that the weight loss effect of berberine might contribute to the inhibition of small intestinal lipid absorption. The possible mechanism was related to the promotion of lacteal junction zippering via suppressing the ras homolog gene family member A (RhoA)/Rho-associated kinase (ROCK) signaling pathway. In vitro, berberine also promoted the formation of stable mature junctions in HDLECs, involving the same signaling pathway.
Berberine could promote lacteal junction zippering and ameliorate diet-induced obesity through the RhoA/ROCK signaling pathway.
肥胖已成为全球性流行病。最近的研究表明，通过促进乳管连接闭合可以预防饮食诱导的肥胖。黄连素是从天然植物中提取的，被发现有减肥的潜力，但具体机制尚不清楚。
确定黄连素是否通过调节乳管连接来预防肥胖，并探讨潜在的分子机制。
在诱导饮食诱导肥胖（DIO）模型后，给予低剂量和高剂量的黄连素 4 周。检测与胰岛素抵抗和脂代谢相关的指标。采用油红 O 染色、透射电镜成像、共聚焦成像等方法观察黄连素对脂类吸收和乳管连接的影响。在体外，用人真皮淋巴管内皮细胞（HDLECs）研究黄连素对 LEC 连接的影响。Western Blot 和免疫染色用于确定相关分子的表达水平。
低剂量和高剂量的黄连素均可减轻 DIO 小鼠的体重，而不抑制食欲，并改善糖脂代谢紊乱。我们还发现，黄连素的减肥效果可能与抑制小肠脂质吸收有关。其可能的机制与通过抑制 Ras 同源基因家族成员 A（RhoA）/Rho 相关激酶（ROCK）信号通路促进乳管连接闭合有关。在体外，黄连素也通过相同的信号通路促进 HDLECs 中稳定成熟连接的形成。
黄连素可通过 RhoA/ROCK 信号通路促进乳管连接闭合，改善饮食诱导的肥胖。
