Effect Of Salidroside On The Myocardial Mitochondria Function Of Rats After Acute Exhaustive

Objective：Mitochondria are organelles that provide cells with energyin eukaryotic cells, also are the main places for cell respiration. Its throughthe electron transport respiratory chain will convert food into chemicalenergy,and the energy stored in the form of ATP for cell use. Through theestablishment of a single bout of exhausted swimming model, our work is toresearch the rat myocardial mitochondrial morphology, and mitochondrialrespiratory rate after exhaustive exercise. In order to investigate the effects ofSalidroside on Mitochondrial function of rats after acute exhaustive.Methods：1A total of40health male Sprague-Dawley rats were randomly dividedinto four groups(n=10in each group), including sedentary control group,exhausted group, low-dose SAL group, high-dose SAL group. Each groupwas administered with low-dose SAL (100mg/kg), high-dose SAL (300mg/Kg)or saline intragastrically for14days. Rats were killed immediately after singlebout of exhausted exercise (Thomas exhausted standardization) besidessedentary control group which were killed in resting state during the sameperiod.2Myocardium samples were taken to observe histomorphologic changesby light microscope and electron microscope afterwards.3ELISA study for concentration of cTnI、CK、MB in plasma andmyocardial tissue.4The state3respiratory ability and state4respiratory ability of themyocardial mitochondrial Complexe Ⅰ with glutamate and malate assubstrates, state3respiratory ability of the myocardial mitochondrialComplexe Ⅱ with succinate as substrate，state3respiratory ability of themyocardial mitochondrial Complexe Ⅳ with TMPD and Ascorbate. were measured by high-resolution respirometry in order to compared theRespiratory Control Ratio (RCR).Results:1Histomorphology of myocardium samples observed by light andelectron microscopy: cardiac sarcomeres of Group Control rat were arrangedin neat rows, the density was uniform and there was no organelle edema,mitochondrial membrane and ridge were normal; The perinuclear matrix ofmyocardium of Group Exhausted suffered a high degree of edema and widerperinuclear gap. the number of mitochondria and glycogen reducedsignificantly. Part of the ridge and part of membrane mitochondria ofperinuclear matrix fused, blurred or missed, a small amount of myocardiumunderwent fiber necrosis. In Group Low-SAL and High-SAL, part of the ridgeand part of membrane mitochondria of perinuclear matrix fused, blurred ormissed.2Serum cTnI assay results: Compared with control group（151.98±8.69ng/ml）, there are no significant defferences in high-does group（158.73±9.82ng/ml）and low-does group（160.29±14.63ng/ml）(P＞0.05)，but the exhausted group（178.86±15.40ng/ml）are significant highter(P＜0.05).3Serum CK assay results: Compared with control group（11.42±0.84ng/ml）,the high-does group（13.65±0.64ng/ml）、low-does group（15.09±0.50ng/ml）and exhausted group （17.20±0.72ng/ml）are all significanthigher(P＜0.05).4Serum MB assay results: There were no significant difference betweenhigh-does（3.55±0.32ng/ml） group and control group （3.90±0.43ng/ml）(P＞0.05).the low-does group and exhausted group are all significant higher(P＜0.05).5State4respiratory ability of the myocardial mitochondrial ComplexeⅠ:There are no significante difference in each group(P＞0.05).6State3respiratory ability of the myocardial mitochondrial ComplexeⅠ: Compared with control group（110.08±9.65pmol.s-1mg-1）,the high-does group （84.88±11.29pmol.s-1mg-1）、 low-does group70.98±7.06pmol.s-1mg-1）and exhausted group（50.14±8.01pmol.s-1mg-1are all significantdecreased(P＜0.05).7Respiraory control raito of the myocardial mitochondrial ComplexeⅠ:Compared with control group（5.43±0.29）,the high-does group(3.75±0.23)、low-does group(2.89±0.19)and exhausted group(1.97±0.26) are all significantdecreased(P＜0.05).8State3respiratory ability of the myocardial mitochondrial ComplexeⅡ: Compared with control group（163.80±18.59pmol.s-1mg-1）, There are nosignificante difference between in high-does group （170.08±26.58pmol.s-1mg-1）(P＞0.05), but the low-does group（117.66±15.21pmol.s-1mg-1）and exhausted group（111.18±40.82pmol.s-1mg-1）are significante decrease(P＜0.05).9State3respiratory ability of the myocardial mitochondrial ComplexeⅣ:Compared with control group（695.45±35.10pmol.s-1mg-1）,the high-doesgroup （535.07±73.11pmol.s-1mg-1）、low-does group（423.04±36.78pmol.s-1mg-1）and exhausted group （382.14±51.64pmol.s-1mg-1）are allsignificant higher(P＜0.05). the high-does group is higher than low-dosegroup and exhausted group(P＜0.05).Conclusion:1Exhaustive exercise would damage the form and structureof mitochondria in rats, resulting in myocardial injury. Its mechanism may bethrough reducing the activity of mitochondrial respiratory chain Complexe,Reduce the respiratory function of mitochondria.2The effects of salidroside on exhaustive exercise resulted in a protectiverole in myocardial and mitochondrial injury, and this effect is dose dependent,The mechanism may be that salidroside increases the activity of complex ofmyocardial mitochondrial respiratory chain in rats, improved myocardialmitochondrial respiratory function, Thus play a protective effect onmyocardium.