Objective: To observe the effect of electroacupuncture (EA) and moxibustion (Moxi) pretreatment on expression of myocardial heat shock protein (HSP) in acute myocardial ischemia-reperfusion injury (MIRI) rabbits.
Methods: A total of 72 New Zealand rabbits were randomly divided into 4 groups:sham operation, MIRI model, EA pretreatment and Moxi pretreatment (n=18 rabbits in each group) which were further divided into 0, 24 and 48 h (time-point) subgroups (n=6 in each). The MIRI model was established by occlusion of the anterior descending branch (ADB) of the left coronary artery for 40 min and reperfusion for 60 min. EA and Moxi stimulation was respectively applied to bilateral "Neiguan"(PC 6) for 20 min, once daily for 5 days before ADB occlusion. The expressions of myocardial HSP 27, HSP 70 and HSP 90 were detected by immunohistochemistry. The pathological and ultrastructural changes of left ventricular ischemia tissue were observed under light and transmission electronic microscope (TEM), respectively.
Results: Outcomes of H.E. staining and ultrastructure showed that MIRI-induced changes of disordered arrangement of cardiomyocytes, vague myocardial transverse striation, inflammatory infiltration, cardiac myofibre necrosis and fibrolysis (light microscope), and myofiber atrophy, vague and disorder in the arrangement of myofiber, myofilament necrosis, interstitial edema, mitochondrial swelling, microvessel expansion, etc. (TEM) were relatively milder in both EA and Moxi pretreatment groups (48 h). In comparison with the sham group, the expression levels of myocardial HSP 27, HSP 70 and HSP 90 had no significant changes after MIRI at the 3 time-points (P>0.05). In the pretreatment groups, the expression levels of HSP 27 at 24 and 48 h in both EA and Moxi groups, HSP 70 at 48 h in both groups, HSP 70 at 0 and 24 h in the Moxi group were significantly up-regulated compared with the model group (P<0.05, P<0.01). No significant changes were found in the expression of HSP 90 at the 3 time-points in the EA and Moxi pretreatment groups (P>0.05). No significant differences were found between EA and Moxi in up-regulating expressions of myocardial HSP 27, HSP 70 and HSP 90 proteins at the 3 time-points (P>0.05) except HSP 70 at 24 h (Moxi being stronger relative to EA, P<0.05).
Conclusions: EA and Moxi pretreatment has a protective effect on ischemic myocardium in MIRI rabbits, which Feb be associated with their actions in up-regulating myocardial HSP 27 and HSP 70 expression.