“肠-肝”循环使肠道微生物变化和肝脏疾病转归紧密相联，肝脏具有强大再生能力，血管生成是肝再生基本条件，一直是研究热点和难点。然而，肠道微生物对肝脏再生血管形成的影响尚未见报道。我们基于肝脏切除术后肠道菌群16s rRNA测序和血清代谢组学质谱结果，发现高速率再生组中显著升高的血清代谢物S1P与肠道差异菌属Veillonella具有显著相关性，进一步发现S1P拮抗剂显著抑制了小鼠肝切除模型的肝脏再生，同时肝再生组织的血管形成被显著抑制。据此可知，肠道微生物相关代谢物S1P，很可能通过调控血管形成，促进了肝脏再生。拟深入阐明：（1）影响血清中S1P水平的肠道微生物及其代谢物；（2）肠道微生物及其代谢物在肝再生血管形成中的作用；（3）S1P在肠道微生物及代谢物调控肝再生血管形成中的作用；（4）S1P调控肝再生血管形成的机制。预期研究结果对促进肝衰竭后肝功能恢复有深远意义，具有重要临床转化价值。

The presence of the “intestinal-hepatic” cycle closely links intestinal microbial changes with liver disease outcomes. Livers have a strong regenerative capacity, and angiogenesis is the basic condition for liver regeneration. It has always been a hotspot and a difficult point in research. However, the effects of intestinal microbes on the formation of regenerative blood vessels in the liver have not been reported. Based on 16s rRNA sequencing and serum metabolomics mass spectrometry results of intestinal flora after hepatectomy, we found that the significantly elevated serum metabolite S1P in the high-rate regeneration group was significantly associated with the intestinal differential genus Veillonella. Antagonists of S1P were found to significantly inhibit liver regeneration in a mouse hepatectomy model while inhibiting the angiogenesis progress in regenerative liver tissues. Based on this, the intestinal microbial related metabolite S1P should promote liver regeneration by regulating blood vessel formation. The study was designed to clarify: (1) intestinal microbes and their metabolites that affect the level of S1P in serum; (2) the role of intestinal microbes and their metabolites in the formation of hepatic regenerative blood vessels; (3) The role of S1P in the regulation of hepatic regenerative blood vessels mediated by intestinal microbes and metabolites; (4) The mechanism of S1P in the regulation of hepatic regenerative blood vessels. The expected results of the study could have far-reaching significance in improving the therapy of acute and chronic liver failure and display promising clinical value.