endothelial cells in response to ACh in OVX rats receiving
various treatments. The maximum vasodilation in the OVX rats
after 12 weeks was significantly lower than that of sham control
(P < 0.05). Treatment with 17β-estradiol at a dose of 2.5 μg/kg
BW prevented impairment of relaxation in the OVX rats
(Figure 2A). Treatment with C. comosa dried powder at a dose
of 1 g/kg/day and isolated compound D3 at a dose of 100 mg/
kg/day (Figure 2B) as well as the C. comosa hexane extract at a
dose of 500 mg/kg effectively prevented impairment of
endothelium-dependent relaxation in the OVX rats (P <
0.05). Their levels were similar to that observed in the
estrogen-treated group. In Figure 2C, hexane extract at dose of
500 mg/kg BW/day prevented the impairment of relaxation
induced by OVX. However, treatment with hexane extract at
lower doses of 125 and 250 mg/kg BW/day was not sufficient
to prevent the reduction of endothelium-dependent relaxation
induced by OVX. EC50 values of ACh in inducing relaxation
among different experimental groups were not significantly
different from each other. These results indicate that the
sensitivity of relaxation responses to ACh was not altered after
12 weeks of estrogen deficiency.