reduced ability to attenuate peroxide-mediated cell damage
compared to native EC.36 On the other hand, the likelihood
that conjugated-flavanol enters the brain has been considered
low, owing to the increased polarity that reduces its ability to
partition and, therefore, limits its transit through the blood−
brain barrier.17 Therefore, to ascertain the substance basis of
neuroprotective effects of C and EC, the parental molecules of
C and EC in rats’ blood and brain were quantified.
Mean unbound C and EC concentration−time profiles at a
dose of 20.0 mg/kg in the rat blood and brain are presented in
Figure 5. Among them, C and EC in brain samples at 130 and
140 min could not be detected because of the sensitivity of
HPLC-CL analysis. The t1/2 values of C and EC were 12.70 ±
3.76 and 13.67 ± 4.33 min for blood while 33.66 ± 3.68 and
41.67 ± 9.14 min for brain. The maximum brain concentrations
of C and EC were observed after about 20 min of
administration. The mean brain Cmax values of C and EC
were 0.51 ± 0.34 and 0.83 ± 0.45 μg/mL. The main blood and
brain pharmacokinetic parameters of C and EC estimated by
the statistical moment method are given in Table 4. Both C and