In summary, the present study demonstrated that P2Y1R was highly expressed in colonic epithelial cells during colitis, and ADP, an endogenous ligand released at the site of inflammation, could activate P2Y1R and hinder intestinal mucosa repair, while inhibition of P2Y1R could promote intestinal mucosal repair by activating epithelial AMPK and reestablishing intestinal flora homeostasis. The gene discussed is PRKAA1; the disease is colitis.