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. 2023 Feb 28;13(7):776–787. doi: 10.1016/j.jpha.2023.02.010

Fig. 6.

Fig. 6

Carbonate-linked choline-conjugated PTX (PTX-R) behavior in vitro. (A) Dissolution equilibrium curve of PTX-R (n = 3). (B) Plasma concentration-time curve of PTX-R in PTX-R-treated rats (n = 6). (C) Plasma concentration-time curve of PTX in PTX-R- or PTX-treated rats (n = 6). (D) The maximum plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC0→24h) of PTX in PTX-R- or PTX-treated rats (n = 6). (E, F) Uptake of PTX-R (E) and PTX (F) with different inhibitor treatments (n = 3; hemicholinium-3 (HC-3): 100 μmol/L; quinidine, cimetidine: 60 μmol/L; mixed inhibitor: 100 μmol/L HC-3 + 60 μmol/L quinidine/cimetidine). (G–I) Effect of PTX-R on relative cell viability of different cells following treatment with or without HC-3 (100 μmol/L) or mixed inhibitors (LLC: 25 μmol/L HC-3/quinidine/cimetidine; A549, BEAS-2B: 100 μmol/L HC-3 + 60 μmol/L quinidine/cimetidine) (n = 3 to 6). (J, K) The concentration changes of PTX-R (J) and PTX (K) in mice plasma treated with or without bis(p-nitrophenyl) phosphate (BNPP) over time (n = 3). (L) The concentration changes of PTX-R in tissue homogenate of tumor (Lewis lung cancer (LLC)), tumor necrosis (Lewis lung cancer) and mice liver over time (n = 3). Mean ± standard deviation (SD), ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.