The protective mechanism of taurine deoxycholic acid (TCDCA) through LPAR1 regulation in Buga syndrome.

The etiology of Budd-Chiari syndrome (BCS), an uncommon but clinically significant condition, remains unclear. Therefore, this study investigates how taurodeoxycholic acid (TCDCA) influences human umbilical vein endothelial cells (HUVECs) in BCS. Following TCDCA treatment, the proliferation, apoptosis, migration, inflammatory response, and angiogenesis of HUVECs were examined, along with the levels of cAMP. Transcriptomic sequencing was further performed. Silencing LPAR1 in HUVECs was performed to explore its functional role. The results revealed significantly higher LPAR1 levels in HUVECs compared to controls. Silencing LPAR1 inhibited cell proliferation, migration, inflammation, and angiogenesis, while promoting apoptosis and increasing cAMP levels. Clinical samples from BCS patients showed significant upregulation of LPAR1, supporting our in vitro findings. Our findings suggest that TCDCA plays a pivotal role in BCS by regulating LPAR1.