OBJECTIVETo investigate the protective effect of ginsenoside Re on myocardial cells of neonatal SD rat with hypoxia injury, and to explore its mechanism.

METHODSThe primary passage of myocardial cells collected from neonatal SD rats were divided into A group (with ordinary treatment), B group [exposed to hypoxia (1% O2, 5% CO2, 94% N(2)) for 12 hours after being cultured for 48 hours], C group (pretreated with 80 g/L ginsenoside Re for 30 minutes after 48 hours of ordinary culture, then exposed to hypoxia for 12 hours), D group (received the same treatment as used in C group except for using 40 g/L ginsenoside Re), E group (received the same treatment as used in C group except for using 20 g/L ginsenoside Re) according to the random number table, with 6 samples in each group. Myocardial cell supernatants were collected for determination of content of lactate dehydrogenase (LDH) with enzyme linked immunosorbent assay. Fluorescence recovery after photobleaching technique was used to detect gap junction intercellular communication (GJIC). Result was observed by laser scanning confocal microscope. Data were processed with paired t test.

RESULTS(1) Compared with that in B group [(403 ± 22) U/L], contents of LDH in E, D, and C groups were obviously decreased [(255 ± 16), (241 ± 13), (237 ± 24) U/L, with t value respectively 5.1, 5.2, 8.3, P values all below 0.05]. (2) The fluorescence recovery rate in A group was (74.8 ± 3.6)% 10 min after quenching, which was higher than that in B group [(13.2 ± 5.6)%, t = 15.2, P < 0.01]. The fluorescence recovery rate in C, D, and E groups was respectively (39.5 ± 2.9)%, (36.2 ± 3.1)%, and (34.3 ± 3.9)% 10 min after quenching, all higher than that in B group (with t value respectively -6.6, -41.9, 18.3, P values all below 0.05).

CONCLUSIONSGinsenoside Re pretreatment, particularly with a dose of 20 g/L, can protect myocardial cells from hypoxia injury, and the effect may be attributable to inhibition of release of LDH and improvement of the GJIC function.