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Objective: To study the effect of Buyang Huanwu Tang on myocardial energy metabolism in rats with diastolic heart failure (DHF) based on adenosine monophosphate (AMP)-activated protein kinase (AMPK)/peroxisome proliferators-activated receptors α (PPARα) signaling pathway,and investigate its mechanism of action.Method: The 48 SD rats were randomly divided into sham operation group and model group.DHF rat model was established by abdominal aorta constriction method.The successfully modeled rats were randomly divided into model group,Buyang Huanwu Tang group (12.72 g·kg-1·d-1),metoprolol tartrate group (0.004 5 g·kg-1·d-1),with corresponding drugs in each group by intragastric administration.The sham operation group and model group were given with equal amount of deionized water,once a day.After 8 weeks of continuous drug intervention,the contents of adenosine monophosphate (AMP),adenosine diphosphate (ADP) and adenosine triphophate (ATP) in peripheral blood of rats were determined by enzyme linked immunosorbent assay (ELISA).The changes of myocardial mitochondrial ultrastructure were detected by electron microscope.The protein expression levels of AMPK,PPARα and peroxisome proliferator-activated receptor-γ coactivator-1α(PGC-1α) in rat myocardium were detected by Western blot.Result: As compared with sham operation group,the contents of AMP and ADP in model group were increased significantly,and ATP content was decreased significantly (PPPPα and PGC-1α protein in the model group were decreased significantly (Pα and PGC-1α protein in Buyang Huanwu Tang group and metoprolol tartrate group were increased significantly (PConclusion: Buyang Huanwu Tang may improve the energy metabolism of the failed heart and delay the progression of heart failure by improving the structure and function of mitochondria,activating AMPK and up-regulating the expression of AMPK/PPARα signaling pathway.
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Objective To observe the effects of mild hypothermia on the myocardial mitochondrial injury induced by oxidative stress after restoration of spontaneous circulation (ROSC) in rat of cardiac arrest model.Methods Eighteen male Wistar rats were randomly (raudom number) divided into normal temperature group and mild hypothermia group after ROSC.Ultrasound was used to measure the left ventricular ejection fraction (EF),shortening fraction (FS) and stroke volume (SV).The levels of glutathione (GSH),malondialdehyde (MDA) and adenosine triphosphate (ATP) in myocardium were detected.The ultramicroscopic structure of myocardial mitochondria was observed under transmission electron microscope at 4 h after ROSC.Results There were no significant differences in basic life support (BLS) time,dosage of epinephrine and number of defibrillation attempt between two groups (P ＞ 0.05).The concentrations of GSH and ATP in myocardium of rats in hypothermia group were significantly higher than those in normal temperature group,while the level of MDA was significantly lower in hypothermia group than that in normal temperature group.Echocardiographic findings showed that hypothermia could significantly improve the EF,FS and SV after ROSC.The hypothermia decreased the myocardial mitochondria injury rather than normothermia [mitochondrial injury score:(0.21-±0.04) vs.(0.42 ±0.08),P ＜ 0.05].Conclusions In this model,mild hypothermia can decrease myocardial oxidative stress injury,improving the cardiac function after ROSC.
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Objective:To investigate the changes of myocardial energy production in septic mice after a cecal ligation and puncture,and to observe the intervention effects of Shenfu injection.Methods:Mice models of abdominal infection were established by a cecal ligation and puncture(CLP).Eighty-three mice were randomly divided into three groups:CLP group(infection group),CLP and treated with Shenfu injection group(treatment group)and pseudooperation control group.The morphology and membrane phospholipid of myocardial mitochondria were studied by using transmission electronmicroscope morphometry method.The activities of cytochrome oxidase(CCO)and succinate dehydrogenase(SDH)of myocardial mitochondria were also detected by enzyme cytochemical method.Reversed phase high-performance liquid chromatography(RP-HPLC)was used to analyze contents of myocardial ATP,ADP and AMP.Results:As compared to control group,a large number of mitochondria were damaged in infection group,the apparent mitochondrial membrane phospholipid deletion and localization change were observed,the activities of CCO and SDH in mitochondria declined obviously,and the contents of ATP,ADP as well as AMP declined notably.All of these were obviously improved in treatment group.Conclusion:The myocardial mitochondrial structure destroyed and its functions declined apparently in septic mice.Shenfu injection could protect the myocardial mitochondrial structure and function effectively,improve the myocardial energy metabolism in septic mice also.
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The effects of superoxide dismutase (SOD) on mitochondrial function after hypoxic and reoxygenated perfusions in isolated rat hearts were observed. Significant decreases in respiration control ratio (RCR) and ADP/O ratio (P/O) as well as activities of succinic dehydrogenase (SDH) and cytochrome oxidase (CCO) were found alter 40 minutes' hypoxia and 20 minutes' reoxygenated perfusion. Adding SOD to the perfusion fluid during the reperfusion period could restore the decreased mitochondfial function, which was shown by increased RCR and P/O as well as activities of SDH and CCO.
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Three groups of Sprague-Dawley rats were fed on low-Se diet frow Keshan disease area, Se-supplemented diet and stock diet respectively, for observing the effect of Se on mitochoadrial monoamine oxidase (MAO) activities in myocardia. The results showed that cardiac mitochondrial MAO activities in the Se-deficient group were significantly decreased as compared to both the Se-supplemented and stock diet group, and Se content in plasma and GSH-Px activity in. red blood cells also were significantly reduced at 30, 60 and 90 days of feeding. In Se-supplemented group MAO and GSH-Px activities as well as Se content were comparable to levels in the stock diet group.