[Effect and mechanism of methyl protodioscin in protecting cardiomyocytes against anoxia/reoxygenation injury].

OBJECTIVE: To study the effect and mechanism of methyl protodioscin (MPD), an active ingredients of yamogenin, in protecting cardiomyocytes (CMC) against anoxia/reoxygenation (A/R) injury. METHODS: Cultured CMCs of neonatal SD rats were randomly divided into three groups, cells in Group A were untreated normal cells, cells in Group B and C were made to injury CMC model by A/R, and only those in Group C were treated with MPD. Levels of ATPase activity and lactate dehydrogenase (LDH) in cell membrane of CMCs were determined. Besides, the mRNA expression of sodium-calcium exchanger (NCX) in MPD treated CMCs was detected. RESULTS: As compared with Group B, the degree of CMC injury was significantly milder and the activities of Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase were higher in Group C after cells were treated with MPD in concentration of 10 microg/mL and 50 microg/mL. The mRNA expression of NCX in CMCs was down-regulated after MPD treatment (P < 0.05). CONCLUSION: MPD could maintain the low calcium internal environment in CMCs by way of protecting the membranous function of Na+ -pump and Ca2+ -pump, and influencing the Ca2+ transmembrane transportation in CMCs.

[Effects of methyl protodioscin on [Ca2+]i and ATPase activity in cardiomyocytes and analysis of mechanisms].

OBJECTIVE: To study the effects of methyl protodioscin on the [Ca2+]i and the ATPase activity in cardiomyocytes, as well as their mechanisms. METHOD: The cardiomyocytes were randomly divided into three groups, the control group treated with no serumal DMEM, the MPD group treated with MPD and the dilthiazem group treated with dilthiazem. Fluorospectrophotometer was used to determined the level of myocardial cell intracellular Ca2+ [Ca2+]i. In the experiment of ATPase activity on cellular membrane, the cardiomyocytes were randomly divided into two groups, the control group treated with no serumal DMEM, the MPD group treated with MPD. The activity of Na+-K+-ATPase,Ca2+-Mg2+-ATPase and Mg2+-ATP ATPase were determined. The quantitative analysis of SERCA2a mRNA expression was studied by RT-PCR that the groups and treatments in cardiomyocytes same as the experiment for ATPase activity assay. RESULT: Under the quiescent condition, compared to the control group, the level of [Ca2+]i in cardiomyocytes of the MPD group and dilthiazem group was no different. After treatment with 40 mmol x L(-1) KCl, [Ca2+] was significantly lower in the MPD group and the dilthiazem group, and the intensity of peak value in time course of 60 s, the dilthiazem group and the MPD group also were lower than the control group (P < 0.001). Ca2+-Mg2+-ATPase and Na+-K+-ATPase in cultured rat were increased after treated with MPD compared to treatment with no serumal DMEM (P < 0.05, P < 0.01), but Mg2+-ATPase in these groups had no different. The expression of SERCA2a mRNA between the MPD group and the control group was no different. MPD could not up-regulated or down-regulated SERCA2a in endocytoplasmic reticulum. CONCLUSION: Methyl protodioscin could block the volt dependent form calcium channel in cellular membrane, and up-regulate the function of sodium pump and calcium pump, so that it could remain low calcium in the internal environment in cardiomyocytes.

[Effects of Panax notoginseng saponins on long-term potentiation in the CA1 region of the rat hippocampus].

Panax notoginseng saponins (PNS) are very important extracts from roots of medicinal herb Sanchi Ginseng which is highly regarded in China for its therapeutic ability to meliorate blood-circulation, anti-anoxia, improve memory, and anti-caducity effects. In this study, we used blind whole-cell voltage-clamp recordings to detect the effects of PNS on long-term potentiation (LTP) in the CA1 region of the hippocampus, and investigated the electrophysiological mechanisms underlying potentiating effects of PNS on learning and memory. Wistar rats (3-4 weeks) were decapitated and hippocampal slices (400 microm thick) were cut coronally. Excitatory postsynaptic currents (EPSCs) were recorded by patch clamp technique in whole-cell configuration. The Schaffer collateral/commissural pathway was stimulated by high frequency stimulation (HFS: 100 Hz) pulses to induce LTP. The findings showed that 0.1 - 0.4 g x L(-1) PNS significantly depressed the amplitude of EPSCs (P < 0.05) and had no facilitative effects on LTP of pyramidal neurons located in the CA1 region. PNS in the concentrations of 0.04 - 0.05 g x L(-1) did not appreciably affect the amplitude of EPSCs (P > 0.05) but markedly increased the amplitude of LTP (P < 0.05). In conclusion, 0.04 - 0.05 g x L(-1) PNS could facilitate LTP in the CA1 region of the rat hippocampus and it is reasonable to suggest that this action may contribute to its potentiating effects on learning and memory.