Curcumin is the yellow pigment of turmeric. In addition to its positive safety profile, curcumin is reported to have beneficial pharmacologic effects as an antioxidant, antitumor, and anti-inflammatory agent, along with other promising pharmacologic effects on the cardiovascular and digestive systems. Curcumin is poorly absorbed, which limits its value in clinical application. In order to improve the poor bioavailability and enhance the pharmacologic action of curcumin, we studied its absorption mechanisms in an animal model in vivo and in a Caco-2 cell model in vitro. The absorption rates of curcumin at different concentrations in blank intestinal juice were not the same. The absorption rate of curcumin solution at a concentration of 5 μg/mL was the highest, followed by 10 μg/mL, and the minimum absorption occurred at 20 μg/mL. The absorption rate in the ileum decreased as the concentration of curcumin increased, which reminds us that absorption in the ileum does not result from simple passive diffusion but rather shows the characteristics of active transport. Curcumin may be a P-glycoprotein (P-gp) substrate and thus may be affected by P-gp efflux, and thus the addition of a P-gp inhibitor such as verapamil can promote the intestinal absorption of curcumin. A Caco-2 cell model was established to accurately study curcumin’s absorption mechanisms. We found that, for curcumin in a 5 μg/mL solution, the Caco-2 cell monolayer transport was passive, and when the concentration was increased to 10 μg/mL efflux influenced the transport but not extensively. The transport mode of curcuminthe appears to be passive diffusion at concentrations <10 μg/mL, but at concentrations >10 μg/mL active transport is involved. In summary, curcumin is transported by a combination of passive diffusion and active transport, curcumin is a substrate for the intestinal transporter P-gp, and intestinal absorption of curcumin is regulated by intestinal P-gp transport.