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Objective:To investigate the protective effect of evodiamine on cardiomyocytes hypoxia injury. Methods:H9c2 myo-cardial cells were exposed to hypoxia for 24 h to induce myocardial cell injury model. The cells were pretreated with different concentra-tions of evodiamine for 12 h. The cardiomyoctes viability was detected by CCK-8 assay. The transcription of inflammatory cytokines was detected by RT-PCR. The cardiomyocyte apoptosis was detected with Tunel staining. The alteration of signal pathway was detected by immunoblotting. Results:Four concentrations of evodiamine did not affect the activity of cardiomyocytes in the basal condition (P>0.05). After 24-hour hypoxia,the viability of cardiomyocytes decreased significantly when compared with that in the control group with significant difference (P<0.05) among 1,5 and 10 μmol·L-1evodia in a dose-dependent manner. The transcription of pro-inflam-matory cytokines(TNF-α,IL-1 and IL-6) significantly increased and the cells apoptosis increased. Evodiamine pretreatment increased the cell viability after hypoxia injury, reduced the transcription of inflammatory cytokines and reduced the number of apoptotic cells when compared with that in the control group with significant differences(P<0.05) between 1 μmol·L-1and 10 μmol·L-1evodia. The results of western blot showed that evodiamine activated AMPKα and AKT, inhibited the activity of NF- kappa B, and compared with the control group,there were significant differences(P<0.05) between 1 μmol·L-1and 10 μmol·L-1of evodia. Conclusion:Evodiamine can protect cardiomyocytes from hypoxia injury and may become a new anti-myocardial ischemia drug.
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<p><b>OBJECTIVE</b>To explore the impact of electroacupuncture (EA) on the protein expression of adenosine receptors in the heart of the rats with myocardial ischemia (MI).</p><p><b>METHODS</b>Thirty healthy male SD rats were divided randomly into a control group (=6), a model group (=12) and an EA group (=12). We ligated the left anterior descending artery (LAD) for MI model in the model group and EA group, and exposed the heart after opening the chest without ligation in the control group. EA, 2 Hz /15 Hz and 1.5-2 mA, was applied at bilateral"Neiguan"(PC 6) in the EA group for 20 min, once a day for continuous 5 days. No intervention except grabbing and fixation was used in the control group and model group. We applied 2% TTC staining to observe the infarct size of myocardium, colorimetry to analyze serum lactic dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB), radio-immunity assessment to detect cardiac troponin T (cTnT), Western blot to evaluate the adenosine A1 receptor (A1AR), A2aAR, A2bAR and A3AR.</p><p><b>RESULTS</b>After treatment, myocardial infarction of (27.56±3.24)% was obvious in the model group; the myocardial infarction in the EA group was (21.04±3.61)%, with statistical significance (<0.05). The expressions of serum LDH, CK, CK-MB and cTnT levels in the model group increased compared with those in the control group (all<0.01), and the expressions of LDH, CK, CK-MB and cTnT levels in the EA group decreased compared with those in the model group (<0.05，<0.01). The A1AR expression in the model group was not different from that in the control group (>0.05), and A2aAR、A2bAR、A3AR expressions decreased (<0.05,<0.01). A2aAR and A2bAR expressions in the EA group increased compared with those in the model group (both<0.01), and there was no statistical significance between A1AR and A3AR expressions (both>0.05). .</p><p><b>CONCLUSION</b>EA may achieve cardioprotective effect by regulating the expressions of A2aAR and A2bAR in myocardial tissue, which induce the corresponding signal cascade for reducing myocardial infarction area.</p>
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Objective To study the protective effect of total glucosides of Mudan cortex(TGM) on acute myocardial ischemia in mice and its mechanism. Methods The total of 60 mice were randomly divided into 5 groups (n = 12),normal control and model control (were given equal capacity of 0.9% sodium chloride solution),and TGM at low,middle,high dose (were given with 50,100,200 mg?kg-1 TGM).The mice were administered once daily for consecutive seven days.After the last administration,the mice in the model control and drug groups were treated by intraperitoneal injection of 15 mg ? kg-1 isoproterenol to to make myocardial ischemia animal model. TGM on the T wave and J point on ECG, and serum lactate dehydrogenase (LDH),myocardial tissue superoxide dismutase (SOD),malondialdehyde (MDA) changes was detected,and the extent of myocardial ischemic injury in mice was measured by Nagar-Olsen staining. Results TGM significantly reduced the displacement of ECG T wave and J point,and improved the related biochemical indexes in mice with myocardial ischemia.The activity of LDH [(898.992± 285.108) μmol?mg-1 ] ,the content of MDA [(11.737 ±5.162) nmol?mg-1 ]in mice treated with TGM at high dose obviously decreased in comparison to the model controls,and the activity of myocardial SOD [(45. 505 ± 20.711) U?mg-1 ] significantly elevated compared with the model control.It was showed that TGM significantly diminished the areas of cardiac muscles ischemia injured via Nagar-Olsen staining. Conclusion TGM has the remarkable protective effect on acute myocardial ischemia injury in mice.
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60 minutes. There were no significant differences in the three groups in age, sex ratio, C/T ratio, or left ventricular function. Blood samples for analysis were collected before skin incision and at time intervals up to 6 days postoperatively. Analysis of creatine kinase MB, LDH and cardiac-specific troponin I was used for the detection of myocardial damage. Meantime, the ECG was checked for myocardial infarction. After the reperfusion, myocardial tissue was obtained from the free wall of right ventricle myocardial structure studies. Results: The level of cTnI was increased significantly when the time of myocardial ischemia was prolonged. The changes of CK-MB and LDH were not significant in these three groups. Electron microscopy demonstrated the mitochondria of myocardial cell swelled, the myofilament shortened and the sarcoplasmic reticulum vacuolated in group III. The ECG was almost normal in all groups. Conclusion: The cTnI was an early and highly sensitive biochemical marker of ischemic and reperfusion injury during correction of cardiac defects in children. The concentration of cTnI was correlated ischemia with the degree of so evaluation of the release of cTnI could be used to assess myocardial protection during cardiac operation.