| For the past few years, study show apoptosis induced by ischemic-reperfusion injury(IRI). In the process of treatment cardiovascular diseases, IRI induced by new and popular therapeutic measure. Protective of myocardial induced by ischemic-reperfusion in rats is researching in cardiovascular diseases. Utilizing the model detective techniques, such as serology, immunohistochemistry and optical microscope, etc. The paper observes the effect of the treatment of TIAN XIN TANG (TXT), and surveys the change of myocardium zymogram, oxidative stressor, albumen expression of apoptosis controlling gene and cadiocyte Cellular Structures to prove the synthetic accommodation action and provide a basis for further utiliza- tion.Objective: To study the protective effects and mechanism of HXT on expeirmental myocardial ischemic-reperfusion rats.Methods: 50 healthy male Wister rats were randomly divided into groups namely blank group, model group, Cedocard group, TXTmax and TXTmin group, 10 rats in each group. Each rat had been recordâ…¡electrocardiographic (ECG) before the experiment. After gaining statistical significance, then saline were given to Blank group and Model group at 10ml/kg weight; suspension of Cedocard were given to Cedocard group at 5mg/kg weight; TXT were given to TXTmax and TXTmin group at dose of 46.6g/kg and 23.3g/kg weight. All of these medicines were administra TXT to rats at 10ml/kg weight and one time each day. The administration would continue 7 days. Until the 8th day, PIT (1U/kg) was injec into rats sublingual vein except Blank group to cause myocardial ischemia and the rats of Blank group were received an equal volume of saline instead of PIT. After 30 minutes all of the rats were to recordâ…¡ECG, then Nitroglycerin was injecting to cause reperfusion injury and the rats of Blank group were received an equal volume of saline instead of NG. After 80 minutes Nitroglycerin was injecting,All of the rats were anaesthetized. The rats were killed and the sera were collect to determine the myocardium zymogram (CK and LDH), oxidative stressor(superoxide dismutase and Malondialdehyde). HE staining was employed to analyze the pathological damage in myocardium of heart apex and SP staining to detect the expression of Bcl-2 and Bax in the myocardium.Results:1 ECG: Compared with the ECG before PIT injection, the ST segments and T waves were changed clinically in all groups except Blank control group, which proved that the animal model was successfully copied. Compared with Blank group, the ST segments and T waves of Model group were decreased most obviously (P<0.01). Compared with Model group, Cedocard, TXTmax and TXTmin group could alleviate the myocardial change of ECG (P<0.01), Compared with Cedocard, TXTmax and TXTmin group could alleviate the myocardial change of ECG significantly (P < 0.01), but the difference between TXTmax and TXTmin group was no statistical significance (P>0.05).2 Myocardium zymogram: Compared with Blank group, the contents of creatine kinase (CK), and lactate dehydrogenase (LDH) in Model group increased significantly (P<0.01). The results showed that zymogram of Cedocard, TXTmin and TXTmax group were significantly lower than Model group (P<0.01). The difference of Myocardium zymogram was no statistical significance in Cedocard, TXTmin and TXTmax group (P>0.05).3 SOD, MDA: Compared with Blank group, the contents of MDA in Model group increased significantly (P<0.01). The results showed that MDA of Cedocard, TXTmin and TXTmax group were significantly lower than Model group (P<0.05 or P<0.01). The difference of MDA was no statistical significance in Cedocard, TXTmin and TXTmax group (P > 0.05). Compared with Blank group, the contents of SOD in Model group decreased significantly (P<0.01). The results showed that SOD of Cedocard, TXTmin and TXTmax group were significantly heighten than Model group (P<0.05 or P<0.01). The difference of SOD was no statistical significance in Cedocard, TXTmin and TXTmax group (P>0.05). 4 Pathological changes: Obviously pathological damage had not be seen in tissue of Blank group, and in Model group, major included pathological changes of focal in most cardiac muscle, swelling and breaking in muscle fiber, vacuolar degeneration, interstitial edema and infiltration of inflammatory cells. The changes of isosorbide dinitrate and TXTmin group were slighter than those in Model group and only included muscle fiber swelling, focal breaking, few vacuolar degeneration and infiltration of inflammatory cells. The pathological changes of TXTmax group were the slightest and most were infiltration of inflammatory cells.5 Expression of Bcl-2 and Bax: Compared with Blank group, the Expression of Bcl-2 and Bax in Model group increased significantly (P<0.05 or P<0.01). The results showed that the Expression of Bax of Cedocard, TXTmin and TXTmax group were significantly lower than Model group. The expression of Bax in TXTmax group was lower than Cedocard, TXTmin group (P<0.01). The difference of the Expression of Bax was no statistical significance between Cedocard, TXTmin group (P>0.01). The results showed that the Expression of Bcl-2 of Cedocard, TXTmin and TXTmax group were significantly heighten than Model group. The expression of Bcl-2 in TXTmax group was better than Cedocard, TXTmin group (P<0.01). The difference of the Expression of Bcl-2 was no statistical significance between Cedocard, TXTmin group (P>0.01).Conclusion: Injection of TXT can protect myocardium damage induced by I/R injury. The mechanism of TXT protection may be associated with inhibiting apoptosis of myocardium, upregulating protein expression of Bcl-2 gene and downregulating protein expression of Bax gene. |
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