There were some previous studies related to GBE50 heart protection activities. Want et al. reported
2+
that GBE50 has inhibitory effects on DADs and TA induced by ouabain and high Ca in guinea pig
papillary muscles [38]. Bao et al. reported that GBE50 could relieve arrhythmia following I/R and
alleviate I/R injury possibly by inhibiting free radicals [39]. Zhang et al. reported that GBE50 could
promote expression of the antiapoptotic gene bcl-2 and bcl-xL in rabb itmyocardium [40]. In the
present study, we investigated the effect of GBE50 on I/R-induced cardiac injury. Administration of
GBE50 at the onset of reperfusion improved the physiological functions of the heart as a result of
the increased HR and decreased S-T height. Acute injury in the form of ischemia leading to production
of inflammatory mediators precipitates into myocardial functional suppression [41,42]. MPO, a
polymorpho nuclear neutrophil derived heme protein, is a biomarker index for neutrophil infiltration
and inflammatory reactivity. Role of MPO activity in myocardial reperfusion injury is well
established [43,44]. The MPO activity in the present study showed steep increment in I/R animals.
This indicated that white blood cell count was sharply increasing in ischemia myocardium tissue.