Camellia Saponin Protective Effect Of Preconditioning In Isolated Rat Hearts During Hypoxia / Reoxygenation Injury

[Background] ischemic preconditioning (IPC) refers to aphenomenon in wh j ch the myocardium is made resistant to pro1ongischefIlia by exposing to brfief pefriods of ischie1nia befote thesubsequent i nsult. The possible mechanism of IPC has beendemonstrated that its cardioprotect ive effects generat ion isby inducing endogenous cardioprotective substance, such asAdenosifle. A1'I'--sensfi tj ve Potassium chanrle1, PKC, BK, N0 and soon. pf1arnloco1og ical i scl1elnic preconditfi oning (P:Ilj) refers toadlllinis ter\ing (lrugs to j nduce production of endogenouscardi ()protect ive chemi ca1 s or trigger ant ii schemi c injurylnechafli sm in myocard iUIn.[Methods and Resu1tJ Iso1ated perfused rat heart model was usedto observe the protective effects and mechanism of SQS onmyocardia1 anoxia/reoxygenation (I/R) injury. The hearts weresigni ficiantly injLlred by 40 lnin anoxia fo11owed by 30 minreoxygenat i()n as I/R mode1. The hearts were subject to three t imes5 min anoxia and 5 min reoxygenation before I/R as IPC mode1. IPCand SQS 0. 5, 0. 25mg/L administered 10 min before anoxia and 1astedfor 30 lll i n. attennated myocardia1 ce1l and mi tochondria1 Ca2+accumulation; perserve the activi ties of mi tochondria1sarcdemmaI Na+--K+--ATP ase, Ca2'--ATPase; iIl1prove cardiac llluslecontracti 1 ity, 1eft ventricu1ar peak systo1ic pressure (LVSP),e1evate heart rate (I-IR) and coroflary flow(CF); reduce theincidellce or severi ty of ventricu1 ar arrhythmias during 30 minreoxygentiti()n. SQS a11d 1PC caUsed a signi ficf[ant reduction intoxi c:l .i pid perixi de n1alj ndial dehyde (MDA), increased theactivity pf myocardiuln superoxia dismutase (S0D) ) g1utathioneperoxidase (GSII--PX) and the adenosine concentration and decreasecreatine kinase (CK) concentration in the coronary perfusate atthe 5 tl1 n1in ()f reoxygenation. these influses of SQS wereattenflated by g [ iberclamide (a specia1 K#i', channe1s blocker) andmethy1-ene b1ue (a se1etive N0 systhesis inhibitor) and polymycinB(a special PKC inhibitor).[ Conc1uSion] We conclude that: OSQS can effectivelyprotect myocax'dia tfroIn ischemic induced by I/R and theprotection appears to be dose--dependance re1ationsbip. @SQScan antagoni ze Ca2+ over1oad in cardiac I/R l njure. @SQS possessanti--oxygenfree radicals and anti--1 ipid peroxidatiofl. @themechani sIn of SQS P:IP are resembled with 1PC invo1 ing K,i'.,, channa1,N0, PKC.