[Study on material basis of Dracocephalum moldavica for protecting cardiomyocyte against hypoxia/reoxygenation injury by traditional Chinese medicine serum chemical and pharmacological methods].

OBJECTIVE: To study the material basis of Dracocephalum moldavica for protecting cardiomyocyte against hypoxia/ reoxygenation injury by using traditional Chinese medicine (TCM) serum chemical and pharmacological methods. METHOD: The extract of D. moldavica (DME) and its content absorbed into blood were determined, while blank serum and medicinal serum of rats before and after intragastrical administration of DME were also compared by HPLC. The Na2S2O4 or N2-based hypoxia/reoxygenation injury model was established by cultivating primary neonate rat cardiomyocytes or H9c2 cells in vitro. Cell viability, LDH release, T-SOD activity, MDA production and apoptosis were detected to learn the effect of DME, medicated serum and different treatments of medicinal serums under different dosage and action duration of DME on cardiomyocyte against hypoxia/reoxygenation injury. RESULT: Four transitional components of DME absorbed into blood after intragastrical administration were found, three of which were original components and one possible metabolite. Furthermore, compared with the model group or the blank serum group, LDH release and MDA production (P < 0.05, P < 0.01) of DME extracts, medicated serum or different treatments of medicinal serum under different dosage and action duration of DME. However, T-SOD and cell viability were improved significantly (P < 0.05, P < 0.01), while apoptosis of cardiomyocytes were also obviously inhibited. CONCLUSION: The four components absorbed into blood are probably the material basis of DME used for protecting cardiomyocyte agastin hypoxia/reoxygenation injury.

[Discussion on quality control of preparations with cortex moutan in volume I pharmacopoeia of People's Republic of China (2005 edition)].

This article analyzed the quality control of 35 preparations with cortex moutan in volume I pharmacopoeia of People' s Republic of China (2005 edition). The result showed that only 11 preparations selected paeonol in cortex moutan as one of their quality indexes, the others selected other components or none as index. Via discussing problems on quality control in preparations with cortex moutan, it gave some suggestions on index selection for quality control and method selection for the determination of paeonol in preparations with cortex moutan, and provided some references for the revision of pharmacopoeia of People's Republic of China (2005 edition I ).

Antithrombotic activities of aqueous extract from Radix Ophiopogon japonicus and its two constituents.

To provide further pharmacological evidence for its clinical use in thrombotic diseases, the antithrombotic activities of the aqueous extract of Radix Ophiopogon japonicus (ROJ-ext) were studied in mouse and rat models. The results showed that ROJ-ext remarkably decreased length of tail thrombus in mice at 48 h and 72 h after carrageenan injection at doses of 12.5 and 25.0 mg/kg. Meanwhile, ROJ-ext markedly inhibited thrombosis induced by arterial-venous (AV) shunt (silk thread) in rats at doses of 6.25 and 12.5 mg/kg. Furthermore, ROJ-ext and one of its components, ruscogenin, significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP) in rats by oral administration of 12.5 mg/kg or 0.7 mg/kg for three times, however, ophiopogonin D 1.4 mg/kg only showed slight inhibition. On the other hand, ophiopogonin D (0.5-2.0 mg/kg, p.o.) and ruscogenin (0.25-1.00 mg/kg, p.o.) produced dose-related inhibition of venous thrombosis induced by tight ligation of the inferior vena cava for 6 h in mice by once oral administration. The findings of this study indicate that an aqueous extract of Radix Ophiopogon japonicus (ROJ-ext) exerted significant antithrombotic activity and ruscogenin and ophiopogonin D are two of its active components, which supported its therapeutic use for thrombotic diseases.

Luteolin inhibits ROS-activated MAPK pathway in myocardial ischemia/reperfusion injury.

AIMS: Luteolin is a falconoid compound that has an antioxidant effect, but its contribution to ROS-activated MAPK pathways in ischemia/reperfusion injury is seldom reported. Here, we have confirmed that it exhibits an antioxidant effect in myocardial ischemia/reperfusion injury (MIRI) by inhibiting ROS-activated MAPK pathways. MAIN METHODS: We exposed rat hearts into the left anterior descending coronary artery (LAD) ligation for 30min followed by 1h of reperfusion. Observations were carried out using electrocardiography; detection of hemodynamic parameters; and testing levels of lactate dehydrogenase (LDH), creatine kinase (CK), total superoxide dismutase (T-SOD), and malondialdehyde (MDA). Mitogen-activated protein kinase (MAPK) pathway was measured by western blot and transmission electron microscopy was applied to observe the myocardial ultrastructure. Rat H9c2 cell in 95% N2 and 5% CO2 stimulated the MIRI. Oxidation system mRNA levels were measured by real-time PCR; mitochondrial membrane potential and apoptosis were measured by confocal microscopy and flow cytometry; western blot analysis was used to assay caspase-3, -8, and -9 and MAPK pathway protein expression; the MAPK pathway was inhibited using SB203580 (p38 MAPK inhibitor) and SP600125 (c-Jun NH2-terminal kinase inhibitor) before H9c2 cells were exposed to hypoxia/reoxygenation injury to show the modulation of the changes in ROS generation, cell viability and apoptosis. KEY FINDINGS: In vivo, luteolin can ameliorate the impaired mitochondrial morphology, regulating the MAPK pathway to protect MIRI. In vitro, luteolin can affect the oxidation system, mitochondrial membrane potential and MAPK pathway to anti-apoptosis. SIGNIFICANCE: These results reveal a ROS-MAPK mediated mechanism and mitochondrial pathway through which luteolin can protect myocardial ischemia/reperfusion injury.

Anti-thrombotic activity of DT-13, a saponin isolated from the root tuber of Liriope muscari.

OBJECTIVE: To investigate the anti-thrombotic activity of DT-13 in experimental animal models. MATERIALS AND METHODS: The anti-thrombotic activity of DT-13 was evaluated by measuring the thrombus induced by inferior vena cava (IVC) ligation in mice and rats. The anti-thrombotic mechanism of DT-13 was investigated by assessing the mRNA expression levels of interleukin-6 (IL-6) and tissue factor (TF) in rat IVC tissue around thrombus. RESULTS: DT-13 markedly inhibited thrombosis induced by IVC ligation for 6 h in mice (2.0 and 4.0 mg/kg, p.o.) and for 18 h in rats (1.4 mg/kg, p.o.). Furthermore, DT-13 down-regulated the increased mRNA expression levels of IL-6 and TF in rats. CONCLUSIONS: DT-13 has an anti-thrombotic activity due to down-regulation of the increased mRNA expression levels of IL-6 and TF.

Effects of bpV(pic) and bpV(phen) on H9c2 cardiomyoblasts during both hypoxia/reoxygenation and H2O2-induced injuries.

Reactive oxygen species (ROS) are involved in myocardial injury. ROS are known to inactivate lipid phosphatase and tension homolog on chromosome 10 (PTEN), an enzyme that increases apoptosis in neonatal cardiomyocytes. BpV(pic) and bpV(phen), two bisperoxovanadium molecules and PTEN inhibitors, may be involved in limiting myocardial infarction. To compare the protective effects of bpV(pic) and bpV(phen) on ROS-induced cardiomyocyte injury and their possible mechanisms, we selected two popular models of hypoxia/reoxygenation (H/R) and H2O2-induced injury in H9c2 cardiomyoblasts to investigate their effects against injury. We found that pre-treatment with bpV(pic) and bpV(phen) increased the viability and protected the morphology of H9c2 cells under the conditions of H/R and H2O2 by inhibiting LDH release, apoptosis and caspases 3/8/9 activities. However, their respective inhibitory abilities in the two models were different, suggesting that the quantity of ROS from the two models might be different. However, the conflict between ROS and PTEN may affect the action of bpV(pic) and bpV(phen). Taken together, the results demonstrate that bpV(pic) and bpV(phen) have inhibitory effects on oxidative stress-induced cardiomyocyte injury that may be partially modulated by the action of ROS on PTEN.