| Background and aimAngiocardiopathy has long been one of the major threats to human health, and coronary heart disease (CHD), with its incidence rate and death rate both at the top of the lists, is claiming an increasing number of lives these years. As the foundational pathology process of CHD is myocardial ischemia, hemoperfusion to the ischemic myocardium is the primary measure taken by the doctors to efficiently prevent further injury to the ischemic heart muscle as soon as possible. It is impossible for myocardial tissue that has been experienced ischemia for a certain time to return its normal function and structure after restoration of blood flow. On the contrary, myocardia cell damage becomes more serious, involving in further injury in aspects of ultramicrostructure, function, metabolism, and electrophysiology. It clinically develops into symptoms such as cardiac arrhythmia, hemorrhagic necrosis, heart hypofunction, etc. This process is called Myocardia Ischemia reperfusion injury (MIRI). It is frequently severe complication during coronary artery bypass, percutaneous coronary intervention (PCI) and thrombolytic therapy for myocardial infarction at present. For this reason, researching how to lessen myocardial ischemia reperfusion injury is becoming a vital question for the prevention of Coronary Atherosclerotic Heart Disease and for the clinical cordis interventional therapy.Qidantongmai tabiet (QDTMT), a kind of traditional Chinese medicine, was formulated on the the traditional Chinese theory of Qi-blood and on the years of clinical experience. Clinical evidence proved preventive effects of QDTMT on ischemic heart disease, but the molecular mechanism was still unknown very well, which impeded its application.Present study investigates deeply the protective effect of QDTMT on rat myocardial ischemia-reperfusion injury from proinflammatory cytokine and oxygen free radicals. The purpose of this study is to supply reliable experimental basis for the clinic application of this medicine in prevention and treatment of Coronary Atherosclerotic Heart Disease and interventional therapy.MethodsThe establishment of animal model 36 healthy male SD rats, 220: 250g, were randomly divided randomly into 6 groups, with 6 rats in each group: sham operated control ischemia-reperfusion group (Control),myocardial ischemia-reperfusion group (model),Tianerxin group (Tianerxin). QDTMT low dosage group (QDTMTL),QDTMT middle dosage group (QDTMTM), QDTMT high dosage group (QDTMTH). QDTMT was given to QDTMT groups at the dose of 0.36,1.08,3.24 g / (kg.d); Tianerxin was given to Tianerxin group 5mg / (kg.d); Saline was giyen to black contral group and model group at 10ml / mg weight. After 7-days of consecutive administration, we operated to establish animal model myocardial ischemia-reperfusion (IR), and then collected blood and ischemia myocardial tissue sample under the sterile condition to detect the contents of Tumor necrosis factor-α(TNF-α) and I Interleukin-6 (L-6) and the contents of Lactate dehydrogenase (LDH) and Malonaldehyde (MDA) ,the changes of activity in Superoxide dismutase (SOD).Results1. In the blood serum, the content of TNF-αand IL-6 in model group was significantly higher than that in control graup (P<0.05). While compared with model group, the content of TNF-αand IL-6 in Medication groups were significantly lower (P<0.05). Furthermore, the function of QDTMTH was significantly better than that of Tianerxin group or QDTMTL group((P<0.05).2. In the blood serum, both the activity of LDH and content of MDA in model group increased significantly (P<0.05) than those in control group(P<0.05) and the activity of LDH and content of MDA in Medication groups were higher remarkably than those in control group (P<0.05), but lower significantly than those in model group (P <0.05). Furthermore, the function of QDTMTH was notablely better than that of QDTMTL ((P<0.05); the effect of QDTMTH on MDA was better than that of Tianerxin group and there was no difference on LDH.3. In myocardial tissue, the activity of SOD in model group was lower notablely than that in control group (P<0.05); the activity of SOD in Medication groups were lower significantly than that in control group (P<0.05), but higher significantly than that in model group (P<0.01). The content of MDA in Medication groups were increased significantly than that in control group (P <0.05), but decreased notablely than that in model group (P <0.05). The function of QDTMTH was remarkably better than that of QDTMTL ((P<0.05); the effect of QDTMTH on SOD was better than that of Tianerxin group and there was no difference on MDA.Conclusions1. QDTMT can decrease the concent of TNF-αand IL-6 in rat model of ischemia reperfusion to relieve ischemia/reperfusion injury.2. QDTMT can increase the activity of SOD, while decrease the content of MDA in myocardial tissue and it can reduce the content of MDA and LDH in the blood serum. This indicates QDTMT can lessen the injury from oxygen free radicals.3. The results demonstrate that Qidantongmai tablet provides remarkable protective effects in rat model of ischemia reperfusion, and it is perhaps because QDTMT can reduce the concentration of proinflammatory cytokine (TNF-α,IL-6) to inhibit inflammatory reaction in corpore and can resist of the injury from oxygen free radicals. The function of QDTMTH is significantly better than that of QDTMTL. |
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