Objectives Panax quinquefolium saponins (PQS) protected myocardium from ischaemia reperfusion (I-R) injury, but it remains unknown whether the effect is associated with the suppression of excessive endoplasmic reticulum stress (ERS). Our purpose is to investigate whether the protective effect of PQS is associated with the suppression of excessive ERS.

Methods The model of myocardial I/R injury in vivo was made by occluding the left anterior descending artery for 45 min followed by 24 h of reperfusion in SD rats. Hemodynamics and serum content of cardiac tropoin T (cTnT) were measured. The myocardial infarct size was measured with triphenyhetrazolium chloride (TTC) staining; apoptosis was detected with in situ TDT-mediated dUTP nick end labelling (TUNEL). Western blotting was used to examine the protein expression of the ERS-related proteins, glucose-regulated protein 78 (GRP78), calreticulin (CRT), CCAAT/ enhancer-binding protein homologous protein (CHOP) and caspase-12; and Bax and Bcl-2.

Results Pretreatment with PQS protected myocardium against I-R-induced injury and apoptosis. Compared with the I/R group: in the PQS + I/R group the mean arterial pressure was decreased by 32.0%, left ventricular ± dp/dt max were increased by 64.0% and 35.0%, respectively (P < 0.05); the serum content of cTnT was decreased by 53.3% (P < 0.05); the percentage of AN/AAR value was reduced by 65.5% and the apoptosis rate was decreased by 54.9% (P < 0.05); the myocardial pathological changes were improved; Bcl-2 protein expression was increased by 110.0% and that of Bax was decreased by 47.8% (P < 0.05); Meanwhile PQS attenuated I-R-induced excessive ER stress as evidenced by decreased caspase-12 activation and expression of GRP78, CRT and CHOP. Compared with the I/R group, in the PQS + I/R group CRT protein expression was decreased by 43.4% (P < 0.05); CHOP protein expression and the protein level of cleaved-caspase12 were decreased by 38.6% and 23.7% (P < 0.05).

Conclusions PQS could alleviate myocardial injury from I-R and the underlying mechanism was likely associated with inhibiting excessive ER stress induced by I-R.