Objective To observe the effectiveness of grain-moxibustion in resisting oxidative stress in doxorubicin(DOX)-induced cardiomyopathy rats.Methods Sixty Sprague-Dawley(SD)rats were randomly divided into blank control group(blank group)
cardiomyopathy model(model)group and grain-moxibustion(moxibustion)group
with 20 rats in each one.The cardiomyopathy model was established by intraperitoneal injection of DOX(0.5mg/100g)
once a week for 4weeks.Grainmoxibustion was applied to"Guanyuan"(CV 4)and"Juque"(CV 14)for 5cones
once daily for 4weeks except the Sundays.The rats' heart rate(HR)
left ventricular systolic pressure(LVSP)
left ventricular diastolic pressure(LVDP)
left ventricular pressure maximum rising rate(+dp/dtmax)
left ventricular pressure maximum decline rate(-dp/dtmax)
left ventricular pressure change time(t-dp/dtmax)were detected to evaluate the cardiac function by using aphysiological signal acquisition-analysis system.The pathological changes of the myocardium were observed by optical microscopy after H.E.staining.The activity of serum lactate dehydrogenase(LDH)
and myocardial malondialdehyde(MDA)and serum cardiac troponinⅠ(cTnⅠ)contents were assayed by enzyme-linked immuno sorbent assay kit(ELISA).Results Following modeling
the HR
LVSP
+dp/dtmax
-dp/dtmax
and myocardial SOD activity were significantly downregulated(P<0.05
P<0.01)
while the LVDP
t-dp/dtmax
serum LDH and CK activity and cTnⅠ content
as well as myocardial MDA content were considerably increased in comparison with the blank group(P<0.05
P<0.01).After moxibustion intervention
the decreased HR
LVSP
+dp/dtmax
-dp/dtmax
and myocardial SOD activity levels and the increased LVDP
tdp/dtmax
serum LDH and CK activity and cTnⅠcontent
as well as myocardial MDA content were remarkably suppressed in comparison with the model group(P<0.05
P<0.01).Conclusion Grain-moxibustion can significantly improve the left ventricular function
increase heart rate in cardiomyopathy rats
which may be associated with its effects in reducing myocardial oxidative stress damage by down-regulating the content of MDA and up-regulating SOD activity in the heart.