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Liguzinediol improved the heart function and inhibited myocardial cell apoptosis in rats with heart failure.

ABSTRACT: AIM: Liguzinediol is a novel derivative of ligustrazine isolated from the traditional Chinese medicine Chuanxiong (Ligusticum wallichii Franch), and produces significant positive inotropic effect in isolated rat hearts. In this study we investigated the effects of liguzinediol on a rat model of heart failure. METHODS: To induce heart failure, male SD rats were injected with doxorubicin (DOX, 2 mg/kg, ip) once a week for 4 weeks. Then the rats were administered with liguzinediol (5, 10, 20 mg·kg(-1)·d(-1), po) for 2 weeks. Hemodynamic examination was conducted to evaluate heart function. Myocardial cell apoptosis was examined morphologically. The expression of related genes and proteins were analyzed using immunohistochemical staining and Western blot assays, respectively. RESULTS: Oral administration of liguzinediol dose-dependently improved the heart function in DOX-treated rats. Electron microscopy revealed that liguzinediol (10 mg·kg(-1)·d(-1)) markedly attenuated DOX-induced injury of cardiomyocytes, and decreased the number of apoptotic bodies in cardiomyocytes. Furthermore, liguzinediol significantly decreased Bax protein level, and increased Bcl-2 protein level in cardiomyocytes of DOX-treated rats, led to an increase in the ratio of Bcl-2/Bax. Moreover, liguzinediol significantly decreased the expression of both cleaved caspase-3 and NF-κB in cardiomyocytes of DOX-treated rats. Administration of digitalis (0.0225 mg·kg(-1)·d(-1)) also markedly improved the heart function and the morphology of cardiomyocytes in DOX-treated rats. CONCLUSION: Liguzinediol improves the heart function and inhibits myocardial cell apoptosis in the rat model of heart failure, which is associated with regulating Bcl-2, Bax, caspase-3 and NF-κB expression.

SUBMITTER: Li Y

PROVIDER: S-EPMC4186991 | biostudies-other | 2014 Oct

REPOSITORIES: biostudies-other

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Project description:BackgroundHeart failure (HF) is a complex clinical syndrome and a serious manifestation or late stage of various heart diseases. This study aimed to explore the protective effects and underlying mechanisms of Shenqi Lixin Decoction (SQLXD) in HF.MethodsA HF rat model was induced by intraperitoneal injection of adriamycin (3 mg/kg in the first 3 weeks, 2 mg/kg in the next 3 weeks, once a week, subcutaneous injection, 6 weeks cumulative dose is 15 mg/kg). After 4 weeks of intragastric administration of SQLXD (9.975, 19.95, 39.90 g/kg, once a day, gavage), the indexes of cardiac function were measured by cardiac color Doppler ultrasound, the cardiac muscle structure and pathological changes were observed by transmission electron microscope, hematoxylin-eosin (HE) staining and Masson. The plasma N-terminal B-type natriuretic peptide (NT-proBNP) level and myocardial tissue adenosine triphosphate (ATP) content were detected by ELISA. FITC detected the cardiomyocyte apoptosis rate (CMAR) labeled Annexin V/PI. Expression of B cell lymphoma factor 2 (Bcl-2), Bcl-2 associated X (Bax), cysteine protease-3 (Caspase-3), and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) mRNA in myocardial tissue were detected by real-time PCR (RT-PCR). The expression of Bcl-2, Bax, Caspase-3 and P53 protein in myocardial tissue were detected by Western blot.ResultsCompared to the normal group, left ventricular end systolic diameter (LVSD), left ventricular end diastolic diameter (LVDD), CMAR and the expression of P53 protein, mRNA and protein of Bax and Caspase-3 were significantly increased in model group, while left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), stroke volume (SV) and the expression of Bcl-2 protein, mRNA of PGC-1α and Bcl-2 were significantly reduced. Compared to the model group, LVSD, LVDD, CMAR and the expressions of P53 protein, mRNA and protein of Bax and Caspase-3 in the medium and high dose SQLXD groups and the control group were significantly decreased, while LVEF, LVFS, SV and the expression of Bcl-2 protein, mRNA of PGC-1α and Bcl-2 were obviously increased. Pathological findings by transmission electron microscope, Masson, and HE staining all revealed protective effects of SQLXD on heart.ConclusionsSQLXD can effectively protect HF rats' hearts. The potential mechanism may be related to the modulation of the expression of PGC-1α and the mitochondrial apoptosis pathway.

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Liguzinediol improved the heart function and inhibited myocardial cell apoptosis in rats with heart failure.

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