Table 1.
Effect of donor gender, age, smoking and drinking on IC50 of baicalin for CYP1A2 in HLMs mean±SD.
Figure 1.
Inhibition of CYP1A2 activity by baicalin in pooled human liver microsomes.
(A) Lineweaver-Burk plots of the effect of baicalin on formation of acetaminophen in pooled human liver microsomes. Reactions were performed in the presence of phenacetin (12.5, 25, 50, 100, 200 µM) and various concentrations of baicalin (0, 10, 20, 40, 80 µM) in the microsome (0.3 mg/mL). (B) Secondary plot of the slopes from the Lineweaver–Burk plots verse baicalin concentrations.
Table 2.
The Km, Vmax and CLint for CYP1A2 and IC50 of baicalin on CYP1A2 in HLMs (n = 28).
Table 3.
Effects of SNP −3860G>A and −163C>A on IC50 of baicalin for CYP1A2 in HLMs mean±SD.
Figure 2.
Mean plasma concentration–time profile of baicalin combination with phenacetin after i.v. administration baicalin at 450 mg/kg in rats.
Each point represents the mean±SD (n = 11).
Figure 3.
Effects of baicalin treatment on phenacetin pharmacokinetics.
(A) The concentration-time profiles of phenacetin (5 mg/kg,i.v.) after treatment with normal saline (control) or baicalin (450 mg/kg, i.v.) in rats. (B) The changes in concentrations(%)-time profile of phenacetin (5 mg/kg, i.v.) after treatment with baicalin (450 mg/kg, i.v.) compared with control. Each point represents the mean±SD (n = 11).
Table 4.
Pharmacokinetic parameters of phenacetin (5 mg/kg, i.v.) after treatment with baicalin (450 mg/kg, i.v.).
Figure 4.
Plots of percentage of control in pharmacokinetic parameters of phenacetin versus Cmax of baicalin.
Figure 5.
Plots of percentage of control in pharmacokinetic parameters of phenacetin versus AUC of baicalin.
Figure 6.
Effect of baicalin at concentration ranged 0 from to 2000·L−1 on concentration of unbound phenacetin(%) in pooled rat plasma (n = 3).
Total phenacetin concentration was 7·L−1. *indicates a significant (P<0.05) increase in concentration of unbound phenacetin (%) from blank value.