[Effects of electroacupuncture on the expression of adenosine receptors in the heart tissue of myocardial ischemia rats].

OBJECTIVE

To explore the impact of electroacupuncture (EA) on the protein expression of adenosine receptors in the heart of the rats with myocardial ischemia (MI).

METHODS

Thirty healthy male SD rats were divided randomly into a control group (n=6), a model group (n=12) and an EA group (n=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.

RESULTS

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 (P<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 P<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 (P<0.05，P<0.01). The A1AR expression in the model group was not different from that in the control group (P>0.05), and A2aAR、A2bAR、A3AR expressions decreased (P<0.05, P<0.01). A2aAR and A2bAR expressions in the EA group increased compared with those in the model group (both P<0.01), and there was no statistical significance between A1AR and A3AR expressions (both P>0.05). .

CONCLUSION

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.