| Objective: Research by intraperitoneal injection of doxorubicinSprague-Dawley (SD) rats, using its toxic effects on the heart to establish ratmodel of heart failure, while intraperitoneal injection of NaHS, an exogenoushydrogen sulfide (Hydrogen sulfide, H2S for body intervention. The expression ofthe heart ventricles ?3adrenergic receptor (?3-adrenergic receptor, ?3-AR),endothelial nitric oxide synthase (Endothelial nitric oxide synthase, eNOS) andchanges in cardiac myocyte apoptosis of SD rats were observed when heartfailure.Exploring the relationship among exogenous H2S,?3-AR, eNOS,myocardial cell apoptosis and its possible mechanism of cardiac function in heartfailure.Method: Adult male SD rats (n=40) were randomly divided into fourgroups:(1) doxorubicin (adriamyein, ADR) group (n=12), intraperitonealinjection of ADR2.5mg/kg, weekly;(2) ADR+sodium hydrosulfide (NaHS)group (n=12), intraperitoneal injection ADR2.5mg/kg, weekly? NaHS14umoL/kg/day (after injection ADR).(3) group NaHS (n=8), I NaHS14umoL/kg/day.(4) control group (n=8), intraperitoneal injection of saline1.25ml/kg per week. Were injected intraperitoneally administered before and oneweek after the administration of10weeks with a heart echocardiogram detected inrat cardiac cavity diameter.The weights of the whole rats and the heart weremeasured at10weeks after the administration. HE, myocardial tissue H2Scontent determination, immunohistochemistry ?3-AR proteinexpression?reverse transcription-polymerase chain reaction (Reversetranscription-polymerase chain reaction, RT-PCR) method were using to measurethe detection of apoptosis of ?3-AR mRNA, eNOS mRNA expression andTUNEL (TdT-mediated dUTP nick end labeling) in myocardial specimens of the sacrificed animals. The SPSS17.0software was used for data analysis andprocessing.Results:1Compared with the control group, ADR group, ADR+NaHS group of rats lose weight, heart weight/body weight (HW/BW) wassignificantly elevated, LVEDD, LVESD increased, LVFS, LVEF decreasedsignificantly (P <0.05). Compared with the ADR group, ADR+NaHS group nosignificant changed in body weight, heart weight/body weight values decreased(P <0.05); LVEDD, LVESD lower, LVFS, LVEF increased, the difference wasstatistically significant (P <0.05). Compared with the control group, NaHS groupno significant changes in these indicators (P>0.05).2Compared with the controlgroup, HE staining of rat cardiac myocytes ADR group showed significantlywidened the gap, disorganized, partly dissolved fracture. Myocardial edema,cytosolic fraction was dissolved state, nuclear stained visible neutralmononuclear lymphocyte infiltration, telangiectasia hyperplasia. Compared withdoxorubicin group, ADR+NaHS group of these changes was lighter.Compared with the control group, NaHS group had no significant change.Theresults of H2S content of the myocardial tissue compared with the measured ADRgroup show that ADR+NaHS group H2S levels increased, the difference wasstatistically significant (P <0.05).4. Protein ?3-AR immunohistochemical assay,by imagepro-plus software analysis, compared with the control group, ADRgroup, ADR+NaHS group ?3-AR-positive area ratio was significantly increased(P <0.05), NaHS group had no significant change (P>0.05). Compared with theADR group, ADR+NaHS group ?3-AR-positive area ratio decrease (P <0.05)5.RT-PCR to measure ?3-AR mRNA, eNOS mRNA expression. Results Comparedwith the control group, ADR group, ADR+NaHS group ?3-AR, eNOS mRNACt value ratio increased significantly (P <0.05), NaHS group had no significantchange (P>0.05). Compared with the ADR group, ADR+NaHS group of theseindicators were reducing.(P <0.05).6. TUNEL determination of myocardialapoptosis index, compared with the control group, ADR group, ADR+NaHS group values myocardial apoptosis rate increased significantly (P <0.05), NaHSgroup had no significant change (P>0.05). Compared with the ADR group, ADR+NaHS group these indicators reduce (P <0.05).Conclusion:1.Adriamycin cansuccessfully build adriamycin cardiomyopathy heart failure model.2. After usingH2S can reduce the degree of heart failure.3.After using H2S interference,?3-AR and eNOS expression were decreased and myocardial apoptosis wasreduced. H2S may be speculated that by regulating ?3-AR, reduce eNOSexpression, so that the local NO concentration decreased myocardial tissue,inhibiting myocardial apoptosis thereby delaying progression of heart failure, theexact mechanism is unclear and requires further study. |
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