| Background Cardiac hypertrophy is one of the main target organ damages inhypertension, and is also an independent cardiac risk factor of death. Only controllingthe blood pressure can not reverse the cardiac hypertrophy and fibrosis which has beenformed due to hypertension. So we must study the pathogenesis and find suitabledrugs to control blood pressure. Nowadays ,drugs for controlling hypertension havetheir own limits for some adverse reactions. So it is important to look for several drugswhich have good therapeutic effect and little side effect in the long-term treatment.TanshinoneⅡA is the mian lipid soluble component of danshen, a kind oftraditional Chinese drug.Now it has been found that tanshinoneⅡA can alleviatecardiac hypertrophy in isolated heart,reduce the collagen deposition, suppress theexpressioon of protoncogene c-fos, but its mechanism is still unknown.Objective Constructing the model of myocardial hypertrophy in hypertensinve ratscaused by abdominal aorta constriction and compare tanshinoneⅡA with anangiotensin receptor inhibitor-valsartan, explore the molecular biologicalmechanism for tanshinoneⅡA.Methods 32 rats at 9 weeks old, which were suffered from abdominal aortaconstriction, were randomly divided into 4 groups for pharmacological treatment. Thefirst three groups were treated respectively by intraperitoneal injection of either STS(10mg·kg-1·d-1), STS(20mg·kg-1·d-1) or sterilized distilled water (1ml·d-1). The otherone were taken Valsartan(10mg·kg-1·d-1 ) intragastriclly. Another 8 rats, which weresuffered from artificial surgery, were also treated by the intraperitoneal injection ofdistilled water (1ml·d-1) as a blank group. Systolic blood pressure(SBP) ,left ventricular mass index (LVMI) were measured after 8 weeks. The thickness ofposterior ventricular wall (PWD),interventricular septum (IVS) and leftventricular ejection fraction (EF) aslo measured by using echocardiogram. HE, VGand immunohistonchemical staining were used to evaluate the myocardial fiberdimension(MFD) . Expressions JAK1 and STAT3 were assessed by using Westernblot.Results①Compared to the blank group, the SBP, PWD, IVS, LVMI, MFD, the expressions ofJAK1 and STAT3 markedly increased among myocardial hypertrophy in which ratswere suffered from abdominal aorta constriction. But the EF values in all groups werein normal range (P＜0.05). All above suggest that the preparation of model issucessful and the items we messured play some roles in the progress of myocardialhypertrophy.②The PWD, IVS, LVMI and MFD of tanshinoneⅡA treatment (low and high dose)were lower than those in myocardial hypertrophy. All of these give us a sign that thetanshinoneⅡA could postpone the progress of myocardial hypertrophy.③The expression of JAK1, STAT3 in tanshinoneⅡA are also lower than those inmyocardial hypertrophy (P＜0.05). But there are no difference in SBP (P＞0.05) . It suggests that the tanshinoneⅡA can inhibits the expression JAK1 andSTAT3. And the effect was not dependent on blood pressure.④There are no difference in all items we measured between the high dose tanshinoneⅡA treatment and low dose tanshinonⅡA treatment.⑤Compared to the myocardial hypertrophy, all the items we measured are lower in therats taken valsartan intragastriclly. (P＜0.05)⑥Compared to valsartan,the effect of anti-hypertrophy of tanshinoneⅡA is lower.This effect also appeared in suppressing the expression of JAK1 and STAT3.Conclusion JAK/STAT pathway plays an important role in ventricular hypertrophy.TanshinoneⅡA could postpone the progress of myocardial hypertrophy by suppressing the JAK-STAT pathway.
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