Fig. 2: GlcN inhibits drug intestinal absorption by enhancing P-gp efflux activity.

a Viscosity of rat intestinal mucus treated with or without GlcN (50 mg/mL for 30 min) was examined by rheometer. b The tight junctions between intestinal epithelial cells treated with GlcN (250 mg/kg for 20 min) were detected by TEM. Scare bar, 1 μm. The image only represents the results of one biological sample. c Transcellular transport rate of capecitabine in Caco-2 cells treated with the indicated drugs was examined by transwell model. n = 3 biologically independent samples. d Schematic of validating the interaction between GlcN and P-gp through cell uptake and gene knockout. Created in BioRender. Qinghua, W. (2025) https://BioRender.com/c20pkwqe, f Accumulation (e) and efflux (f) of Rh123 in Caco-2 cells treated with or without GlcN at the indicated concentrations were determined by a multimode reader (Ex = 485 nm, Em = 528 nm). n = 6 biologically independent samples. g Expression of P-gp in the indicated Caco-2 cells was determined by immunoblot. h Cellular uptake of Rh123 in control and P-gp silenced Caco-2 cells treated with or without GlcN at the indicated concentrations was determined (Ex = 485 nm, Em = 528 nm). n = 6 biologically independent samples (After-silencing, p-value for Verapamil = 0.3034, 1 mM = 0.9996, 10 mM = 0.7150, 15 mM = 0.9993). i, k Pharmacokinetic behavior of digoxin in wild-type (wt) FVB mice (i) and abcb1^(-/-) mice (k) in the presence or absence of GlcN (500 mg/kg). n = 6 biologically independent mice. j Schematic of the abcb1 gene knockout process in mice. Created in BioRender. Qinghua, W. (2025) https://BioRender.com/c20pkwq. Data are means ± SEM and p-values were calculated using one-way ANOVA in c−h. ^**p < 0.01, ^***p < 0.001, ^****p < 0.0001, NS represent not significant.