| IntroductionThe main pathological mechanisms of myocardial ischemia reperfusioninjury(MIRI)are excessive oxygen free radicals, calcium overload, inflammation,apoptosis and so on. Tianma is a kind of traditional Chinese medicine for a variety ofeffects, and gastrodin (4-hydroxymethyl benzyl alcohol-β-D glucopyranoside) is themost effective single activity. Our previous studies have shown that gastrodinpreconditioning can attenuate myocardium ischemia reperfusion injury by reducinginflammatory cell infiltration and inhibiting calcium overload in rats.Whether thegastrodin reduced the inflammation by affecting the emancipation of the TNF-α andIL-6;Whether the gastrodin inhibited the overload of calcium by affecting theSERCA.Both of them were not reported at abroad.ObjectiveTo observe the possible mechanisms of Gastrodin precondition on attenuatingreaction of MIRI by establishing MIRI model of rat.We research the possiblemechanisms by observing the change of the inflammatory factors and SERCA onmyocardial tissue and serum and the changes of the cell electrophysioogical.MethodsSD rats were healthy and adult.They were randomized into sham group, MIRI group,Gastrodin group of low dose (0.1g/kg), middle dose (0.2g/kg) and high dose (0.4g/kg).Rats were treated via intragastric administration for one week.The MIRI model of rats was established by ligaturing the left anterior descending coronary artery. We can usethe electrocardiogram to identify whether the MIRI model of rats were successful.Thechanges of tumor necrosis factor (TNF-α) and interleukin-6(IL-6) in blood serum andmyocardial tissue were determined according to the kit introduction. The sareoplasmicreticulum Ca2+_ATP (SERCA) in myocardial tissue was determined according to thekit introduction.The myocardial tissues were taken to observe the changes inmyocardial histology and morphology by HE staining.The changes of the sinoatrial node cells and atrial myocytes of sham group, MIRIgroup and gastrodin group(0.1g/kg,0.2g/kg,0.4g/kg) were observed by the myocardialcell bioelectricities techniques. The possible mechanism of gastrodin precondition onattenuating reaction of MIRI in rats.According to the results of electrophysiological recordings, using ion channelblockers to reduce myocardial injury by perfusion the heart of normal rat, and thenanalysis the possible ionic mechanism of gastrodin precondition on attenuating reactionof MIRI in rats.All date was performed using SPSS17.0software. Measurement data was showed asx±s. Comparison between groups used ANOVA and paired t-test, P <0.05wasstatistically significant.Results1. The effect of Gastrodin on ST of rats. Compared with the sham group, the ST ofthe MIRI group was not changed before the LAD was ligationed(P>0.05). But the ST ofthe MIRI group was higher after ischemia and reperfusion(P<0.01).Compared with theMIRI group,the ST of the middle and high concentration were lower after ischemia andreperfusion(P<0.01). 2. The effect of Gastrodin on TNF-α in blood serum and myocardial tissue.Compared with the sham group, the content of TNF-α in blood serum and myocardialtissue were increased significantly in the MIRI group (P<0.01). Compared with theMIRI group,the content of TNF-α in blood serum and myocardial tissue were reduced inthe Gastrodin low-dose(0.1g/kg)(P>0.05), but the content of TNF-α in blood serum andmyocardial tissue were reduced significantly in Gastrodin group of middle and highconcentration(P<0.01).The gastrodin group compared with each other was notstatistically significant(P>0.05).3. The effect of Gastrodin on IL-6in blood serum and myocardial tissue. Comparedwith the sham group, the content of IL-6in blood serum and myocardial tissue wereincreased significantly in the MIRI group (P<0.01). Compared with the MIRI group,thecontent of IL-6in blood serum and myocardial tissue were reduced in the Gastrodinlow-dose(0.1g/kg)(P>0.05), but the content of IL-6in blood serum and myocardialtissue were reduced significantly in Gastrodin group of middle and highconcentration(P<0.01).The gastrodin group compared with each other was notstatistically significant(P>0.05).4. The effect of Gastrodin on SERCA in myocardial tissue. Compared with the shamgroup, the content of SERCA in myocardial tissue were reduced in the MIRI group(P<0.01). Compared with the MIRI group,the content of SERCA in myocardial tissuewere increased in the Gastrodin low-dose(0.1g/kg)(P>0.05), but the content of SERCAin myocardial tissue were increased significantly in Gastrodin group of middle and highconcentration(P<0.01).The gastrodin group compared with each other was notstatistically significant(P>0.05).5. The effect of Gastrodin on the histology and morphology. In the sham group thecardiac cell morphology was complete and arranged in neat rows;in the MIRI group thecardiac cell morphology was edema and telangiectasia obviously,we can see the red blood cells and inflammatory cell infiltration;In the Gastrodin low-dose the cardiac cellmorphologywas edema obviously and the red blood cells and inflammatory cellinfiltration were reminded to be seen;But the cardiac cell morphology was edema andarranged in neat rows obviously in the in Gastrodin group of middle and highconcentration, the number of the red blood cells and inflammatory cell infiltration werelittle.6. The effect of Gastrodin on action potential of sinoatrialnode cells. Compare withthe indicator of AP was changed in the MIRI group.The AFP,Vmax and VDD wereslower(P<0.05). The MDP was elevated and the APA was lower(P<0.05). Comparedwith the MIRI group,the APF,Vmax and VDD were significantly accelerated in theGastrodin group(P<0.01).7. The effect of Gastrodin on action potential of atrial myocytes. Compared with thesham group, the RP was elevated and the APA was lower(P<0.05),the Vmax wasslower(P<0.05).Compared with the MIRI group,the APD50and APD90weresignificantly accelerated in the Gastrodin group(P<0.01).8. The effect of Gastrodin on T-type calcium channel. Compared with the normalsinus,the Mirabelli can accelerate the VDD(P<0.05).Compared with the Mirabelli,theGastrodin can accelerate the VDD(P<0.05).9. The effect of Gastrodin on KATP. Compared with the normal sinus, the DZ canaccelerate the VDD(P<0.05). Blocked by5-HD before using DZ, the effect of DZaccelerate APD90was inhibited. Gastrodin perfusion can shorten APD90(P <0.05),compared with the normal sinus. Blocked by5-HD before using gastrodin, APD90stillshorter, and the difference was statistically significant (P <0.05). Conclusion1. Gastrodin preconditioning can attenuate myocardium ischemia reperfusion injury inrats which maybe related to its anti-inflammation function and the increase of SERCAand the protection of the electrical activity of myocardial cells.2. Gasrodin preconditioning can acceleerate the self-discipline of the sinoatrial nodecells may be unrelated to the opening of T-type calcium channel.3. Gasrodin preconditioning can short the APD90of atrial myocytes may be unrelated tothe opening of KATP. |
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