| Objective Exercise training is an external stimulus that has two-wayeffects on the heart. Aerobic exercise and the low-intensity exercise canproduce good effect on heart, such as muscle fiber swelling and hypertrophy,mitochondria densty compacted, capillary density increased and myocardialcontractility enhanced, etc., but exhaustive exercise or long-term over-traininghas a negative effect on heart, it can damage the normal function of the heartand make the heart to a pathological change. How to prevent exercise-inducedorgan injury is the common problem which sports medicine, military medicineand clinical medicine concerned. Apoptosis and inflammatory response is themain mechanism of overtraining-induced acute myocardial injury, Caspase-1is an important member of the caspase family which play an important role inapoptosis, it can also activate the inflammatory cytokines IL-18mediatinginflammatory response, however the role of Caspase-1IL-18inovertraining-induced acute myocardial injury need to be explored. Studiesshowed that pre-administration of anisodamine can protect cardiocytes byreducing the inflammatory response and myocardial apoptosis. But its effecton Caspase-1and IL-18is not clear. In our study, The animal model ofovertraining-induced acute myocardial injury was produced by exhaustiveswimming. We investigate the role of caspase1and Interleukin-18onovertraining-induced acute myocardial injury in rats and the preventativeeffect of Anisodamine by determining the expressions of Caspase1andInterleukin-18in myocardial tissue.Method1Animal selection and group Forty-eight healthy maleWistar rats weighing200-220g were randomly divided into three groups： control group（C，n=8）, exhaustive swimming group（ES, n=24） andAnisodamine group（AD, n=16, received a single intraperitoneal injection ofAnisodamine at a dose of10mg/kg at20minutes before swimming）.2Theestablishment of animal model ES group and AD group were receivedexhaustive swimming to produce overtraining-induced acute myocardialinjury model. Rats of each group were given adapt swimming30minutes atthe first day,on the second day,they were put into the water till exhausted.Exhaustive criteria:1sink to the bottom for more than10seconds;2swimming action was inconsistent;3there is no escape response whenremoving out of water, and can not complete righting reflexion.3.Collectingsample For ES group,inferior vena cava blood and heart samples werecollected at exhaustive swimming instantly,6,24h and for AD group at6,24h.4Observe index Inferior vena cava blood samples were collected fordetermination serum concentrations of cTnI(by ELISA).Heart samples werecollected for determination the expressions of Caspase1and Interleukin-18inmyocardial tissue (by immunohistochemistry) and pathologic examination(with light microscope). TUNEL were performed to evaluate renal cellapoptosis5Statistical analysis All data were analysized by SPSS13.0statistical software.measurement data were expressed by mean±standarddeviation(ˉx±s), tests of between-subjects contrasts were compared by usingANOVA, P＜0.05was considered statistically significant.Results1Changes of myocardial histopathology HE staining showedthat only part of the myocardial fiber were swollen and hypertrophic，myocardial interstitial blood vessels and capilary dilated in ESI; In ES6h thenucleus of myocardial cells were deep stained, myocardial fiber wereobviously swollen, hypertrophic, disorganized and irregular fracture; inES24h the swell and hypertrophy of myocardial fiber were alleviated,myocardial cells scattered in a large number of inflammatory infiltration foci.Changes in myocardial histopathology were significantly reduced in AD group.2Changes of serum cTnI concentration Compared with group C, theconcentration of serum cTnI was obviously increased in ES group（P＜ 0.05）,and compared with ESI, the concentration of serum cTnI was obviouslyincreased in ES6h, but obviously decreased in ES24h（P＜0.05）. Comparedwith the corresponding time of ES group, the concentration of serum cTnI wasobviously decreased in AD group（P＜0.05）.3Changes of myocardial cell apoptosis there has not seen the obviousmyocardial cell apoptosis in C group; the number of apoptostic cell inmyocardial tissue was increased markedly in ES group,and the number cameto the peak at6hours after exhaustive swimming, the number slightly reducedat24hours. The number of myocardial cell apoptosis obviously reduced inAD rats. Compared with group C, myocardial cell apoptosis rate obviouslyincrease in group ES（P＜0.05）, and compared with ESI, myocardial cellapoptosis rate was significantly increased in ES6h and ES24h（P＜0.05）;compared with ES6h, myocardial cell apoptosis rate was obviously decreasedin ES24h (P <0.05); Compared with the corresponding time of ES group,myocardial cell apoptosis rate were significantly reduced in AD group（P＜0.05）.4Expression levels of Caspase-1and IL-18in myocardial tissueCompared with group C, the expressions of Caspase1and Interleukin-18inmyocardial tissue up-regulated in group ES（P＜0.05）, and compared withESI,the expressions of Caspase1and Interleukin-18was significantlyincreased in ES6h and ES24h （P＜0.05）, compared with ES6h,the expressions of Caspase1and Interleukin-18was significantly decreasedin ES24h （P＜0.05）. Compared with group ES, the expressions of Caspase1and Interleukin-18in myocardial tissue was significantly decreased in groupAD（P＜0.05）.Conclusions1The exhaustive swimming could induced myocardialcell apoptosis, give rise to acute myocardial injury.2Caspase1and Interleukin-18play an important role in overtraining–induced acute myocardial injury rats.3Anisodamine can reduce myocardial injury by down regulating the expression of Caspase1and Interleukin-18in myocardial tissue. |
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