Effect of exercise on improving myocardial mitochondrial function in decreasing diabetic cardiomyopathy.

Diabetic cardiomyopathy (DCM) is a significant cause of heart failure in patients with diabetes, and its pathogenesis is closely related to myocardial mitochondrial injury and functional disability. Studies have shown that the development of diabetic cardiomyopathy is related to disorders in mitochondrial metabolic substrates, changes in mitochondrial dynamics, an imbalance in mitochondrial Ca2+ regulation, defects in the regulation of microRNAs, and mitochondrial oxidative stress. Physical activity may play a role in resistance to the development of diabetic cardiomyopathy by improving myocardial mitochondrial biogenesis, the level of autophagy and dynamic changes in fusion and division; enhancing the ability to cope with oxidative stress; and optimising the metabolic substrates of the myocardium. This paper puts forward a new idea for further understanding the specific mitochondrial mechanism of the occurrence and development of diabetic cardiomyopathy and clarifying the role of exercise-mediated myocardial mitochondrial changes in the prevention and treatment of diabetic cardiomyopathy. This is expected to provide a new theoretical basis for exercise to reduce diabetic cardiomyopathy symptoms.

Regulation of Mitochondrial Dynamics by Aerobic Exercise in Cardiovascular Diseases.

Mitochondrial dynamics, including continuous biogenesis, fusion, fission, and autophagy, are crucial to maintain mitochondrial integrity, distribution, size, and function, and play an important role in cardiovascular homeostasis. Cardiovascular health improves with aerobic exercise, a well-recognized non-pharmaceutical intervention for both healthy and ill individuals that reduces overall cardiovascular disease (CVD) mortality. Increasing evidence shows that aerobic exercise can effectively regulate the coordinated circulation of mitochondrial dynamics, thus inhibiting CVD development. This review aims to illustrate the benefits of aerobic exercise in prevention and treatment of cardiovascular disease by modulating mitochondrial function.

Study on the protective effects of danshen-honghua herb pair (DHHP) on myocardial ischaemia/reperfusion injury (MIRI) and potential mechanisms based on apoptosis and mitochondria.

CONTEXT: Danshen, the dried root and rhizome of Salvia miltiorrhiza Bunge (Labiatae) and honghua, the dried flower of Carthamus tinctorius L. (Compositae) as the herb pair was used to treat cardiovascular diseases (CVD). OBJECTIVE: To study the effects of DHHP on MIRI and mechanisms based on apoptosis and mitochondria. MATERIALS AND METHODS: 36 SD rats (n = 6) were randomly divided into control group (Con), the ischaemia-reperfusion group (IR), positive control (Xinning tablets, XNT, 1 g/kg/d) and DHHP (1.2, 2.4, and 4.8 g/kg/d). Except for Con, the other groups were intragastrically administrated for 5 d, the rat hearts were isolated to establish the MIRI model in vitro for evaluating the effects of DHHP on MIRI. 24 SD rats (n = 6) were randomly divided into Con, IR, DPPH2.4 (2.4 g/kg/d) and DPPH 2.4 + Atractyloside (ATR) (2.4 + 5 mg/kg/d), administered intragastrically for 5 d, then treated with ATR (5 mg/kg/d) by intraperitoneal injection in DPPH2.4 + ATR group, took rat hearts to establish MIRI model in vitro for revealing mechanism. RESULTS: Myocardial infarct sizes were, respectively, 0.35%, 40.09%, 15.84%, 30.13%, concentrations of NAD+ (nmol/gw/w) were 144, 83, 119, and 88, respectively, in Con, IR, DHHP2.4, DHHP2.4 + ATR group. Cleaved caspase-3 were 0.3, 1.6, 0.5 and 1.3% and cleaved caspase-9 were 0.2, 1.1, 0.4 and 0.8%, respectively, in Con, IR, DHHP2.4 and DHHP2.4 + ATR group. The beneficial effects of DHHP on MIRI were reversed by ATR. CONCLUSIONS: The improvement of MIRI by DHHP may be involved in inhibiting MPTP opening, decreasing oxidative damage, alleviating ischaemic injury and inhibiting cardiomyocyte apoptosis.

Effects of Aging on Expression of Mic60 and OPA1 and Mitochondrial Morphology in Myocardium of Tibetan Sheep.

In order to investigate the effects of aging on the expression of Mic60 and OPA1 and mitochondrial morphology in plateau animals, the expression of Mic60 and OPA1 genes and proteins, and the morphology of mitochondria in the myocardium of adult and aged Tibetan sheep were investigated. The expression of Mic60 and OPA1 genes and OPA1 protein were higher (p < 0.05) in the myocardium of adult Tibetan sheep than in those of the aged ones. The number of mitochondrial cristae in the myocardium of adult was higher than that in aged (p < 0.05). The density of mitochondria in the myocardium of adult was higher than that in aged (p < 0.01). Compared with the adult Tibetan sheep, the mitochondrial crista of aged were relatively sparse, the crista membrane was wide, and the mitochondria were not closely linked, showing fragmentation. These results suggest that the myocardial mitochondria of the adult have better energy supply ability, indicating that aging can lead to the weakening of oxygen supply in the myocardial mitochondria of Tibetan sheep.

Effect of Buyang Huanwu Tang on Myocardial Mitochondrial Energy Metabolism and AMPK/PPARα Signaling Pathway in Rats with Diastolic Heart Failure / 中国实验方剂学杂志

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.

Effect of mild hypothermia on the oxidative stress induced myocardial injury after cardiopulmonary resuscitation / 中华急诊医学杂志

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.

Protective effect of Shenfu injection on myocardial energy metabolism in septic mice / 重庆医科大学学报

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.

THE EFFECTS OF SUPEROXIDE DISMUTASE ON MYOCARDIAL MITOCHONDRIA INJURED BY REOXYGENATED PERFUSION / 西安交通大学学报(医学版)

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.

EFFECT OF Se-SUPPLEMENTATION ON MONOAMINE OXIDASE ACTIVITY IN MYOCARDIAL MITOCHONDRIA OF RATS FED ON GRAINS FROM KESHAN DISEASE AREA / 营养学报

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.