3 RESULTS
3.1
Isorhamnetin treatment inhibited AngII-induced AF susceptibility in
mice
To test the inhibitory effects of isorhamnetin on susceptibility to AF,
an AF induction study was performed using a transvenous electrode
catheter. After 30 s of burst pacing, AF was spontaneously induced and
terminated (Fig. 1A). As a result, AngII significantly increased the AF
induction rate and resulted in a longer AF duration than that of the
control group. Isorhamnetin treatment reversed the increase in AF
induction rate and AF duration prolonged by AngII (Fig. 1B-C).
Next,
AERP (basic cycle length (BCL) =150 ms) was measured for the three
groups. Compared with the control group, AngII significantly decreased
AERP, while isorhamnetin reversed this effect. AF induction rate:
Control vs. AngII vs. AngII+isorhamnetin
(4.0%
vs. 34.3% vs. 20.0%); Induced AF duration: Control vs. AngII vs.
AngII+isorhamnetin (0.5 ± 0.4 s vs. 20.4 ± 1.9 s vs. 8.6 ± 1.1 s); AERP:
Control vs. AngII vs. AngII+isorhamnetin (101.7 ± 3.3 ms vs. 64.1 ± 2.4
ms vs. 78.3 ± 2.8 ms).
These results demonstrate that isorhamnetin restored shortened AERP and
suppressed the vulnerability of AF.
3.2
Isorhamnetin suppressed AngII-induced abnormal
diastolic