| Objective: To estimate the pharmacological effect of Cuscuta chinensis Lam.flavonoids (CCLF)against myocardial infarction (MI) in rats and explore its possible mechanisms.Methods: SD rats were divided into six groups at random. They were control group (CK), modelgroup (MOD), propranolol group (PRO), CCLF100mg/kg group, CCLF200mg/kg group andCCLF400mg/kg group. Rats who were in the PRO, CCLF100mg/kg group, CCLF200mg/kg groupand CCLF400mg/kg group were intragastric administration by corresponding drugs for a week bythe gastric volume that is1ml/100g body weigh, and once a day; and rats of CK group andMOD group were gavaged by the same volume of physiological saline. When rats were madeto intragastric administration in last day, After2h, MOD group, PRO group, CCLF100mg/kg group,CCLF200mg/kg group and CCLF400mg/kg group rats were injected with isoprenaline (ISO85mg/kg,1ml/100g) in the abdominal subcutaneous by multiple points, and after24hours, the sameamount of ISO was injected again, in order to establish the model of myocardial infarction; andthe same amount of physiological saline was injected to normal control group. Measuremento f hemodynamic parameters by Powerlab16channel physiological recorder and Millar catheter; Lipidperoxidation level, energy metabolism index and the activity of ATPase enzymes on mitochondrialmembrane were detected in myocardial tissue by ultraviolet spectrophotometer; and change ofhistopathologieal in myocardium were observed by microscope.Results:⑴Compared with CK group, myocardial index (HMI) of MOD group rats increase52.07%, they are significantly difference (P﹤0.01). Compared with the MOD group, HMI ofCCLF100mg/kg and CCLF200mg/kg group rats decrease5.42%and4.40%.⑵Compared withCK group, heart rate of MOD group rats increase12.50%, ST segment of MOD group ratselevate0.09mV, T wave and R wave amplitude go down0.16mV and0.13mV, and they are significantlydifference（P﹤0.05, P﹤0.01）.Compared with the model group, CCLF200mg/kg group rats’ heartrate decrease, ST segment decline, T wave and R wave amplitude rise, they reach significantlydifference（P﹤0.05, P﹤0.01）. The effect of CCLF200mg/kg was the best; the heart rate of CCLF200mg/kg significantly lower than that of MOD group, and it reaches significant difference （P﹤0.05）.⑶For myocardial infarction rats induced by ISO, CCLF200mg/kg could significa-ntly elevated arterial systolic pressure (SP), the left ventricle maximum systolic pressure (LVSP),left ventricular pressure maximum increase/decrease rate (±dP/dt), left ventricular contractility index(CI), strok work (SW) cardiac output (CO), stroke volume (SV), ejection fraction (EF), theyachie-ve largly difference (P﹤0.05, P﹤0.01); decreased remarkably left ventricular enddiastolicpressure (EDP), left ventricular end-systolic volume (ESV), left ventricular end-diastolic volume(EDV), arterial elastance (Ea), myocardial oxygen consumption index (MOCI), total peripheralvascular resistance (TPVR); significantly reduced time constant of left ventricular pressure decay(Tau),they achieves significant difference (P﹤0.05, P﹤0.01). pressure-volume (P-V) loop ofCCLF200mg/kg converged with those of control group. CCLF100mg/kg and CCLF400mg/kg canalso improve some hemodynamic parameters of myocardial infarction rats.⑷CCLF100mg/kg andCCLF200mg/kg can improve remarkably the activity of superoxide dismutase (SOD),glutathione peroxidase (GSH-Px) and catalase (CAT) in damaged myocardial tissue, decreased theactivity of nitric oxide synthase (NOS) and malondialdehyde (MAD) content in damagedmyocardial tissue; significantlyincreased the output of the energy, increased the content of ATP, andreduced the content of free fatty acid (FFA), the activity of Na+/K+-ATPase, Mg2+-ATPase, Ca2+-ATPase and Ca2+-Mg2+-ATPase enzymes on mitochondrial membrane was a significant rise.⑸InThe histopatho-logic morphology, three different doses of CCLF groups can ease myocardialfibrosis damage by MI, especially the effect of CCLF200mg/kg is obvious.Conclusion: this study demonstrates that three different doses of CCLF have a significanteffect in the protection of heart against MI induced by ISO, the effectiveness of CCLF200mg/kgis the best. Its effect pathway and mechanism may be⑴CCLF can alleviate myocardial cellmembrane damage, and stable myocardial cell membrane system, in order to guarantee thedepolarization and repolarization of normal myocardial cells, thereby ameliorating the abnormalitiesof ECG.⑵Enhancing the systolic and diastolic function of the heart, elevating the ability ofheart pump blood and energy efficiency and improving heart function; Decreasing the myocardialoxygen consumption andtotal peripheral vascular resistance, providing oxygen and blood for injuried myocardial to slow downthe occurrence of myocardial infarction.⑶Promoting the scavengingability for free radical, alleviating lipid peroxidation; Raising energy output and the utilization ratio,and providing enough energy for myocardial; increasing the activity of ATPase enzyme onmitochondrial membrane, maintaining the balance of ion concentration of myocardial cell andkeeping cellmembrane stabili-ty.⑷Eliminating the inflammation of myocardial fibers, keeping theintegrity ofmyocardial fibers. |
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