• The Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.45-55
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• 2007

We elucidated the effects of various components of ischemic medium on the outcome of simulated ischemia-reperfusion injury. Hypoxia for up to 12 hours induced neither apoptotic bodies nor LDH release. However, reoxygenation after 6 or 12 hours of hypoxia resulted in a marked LDH release along with morphological changes compatible with oncotic cell death. H9c2 cells were then subjected to 6 hours of simulated ischemia by exposing them to modified hypoxic glucose-free Krebs-Henseleit buffer. Lowered pH (pH 6.4) of simulated-ischemic buffer resulted in the generation of apoptotic bodies during ischemia, with no concomitant LDH release. The degree of reperfusion-induced LDH release was not affected by the pH of ischemic buffer. Removal of sodium bicarbonate from the simulated ischemic buffer markedly increased cellular damages during both the simulated ischemia and reperfusion. Addition of lactate to the simulated ischemic buffer increased apoptotic cell death during the simulated ischemia. Most importantly, concomitant acidosis and high lactate concentration in ischemic buffer augmented the reperfusion-induced oncotic cell death. These results confirmed the influences of acidosis, bicarbonate deprivation and lactate on the progression and outcome of the simulated ischemia-reperfusion, and also demonstrated that concomitant acidosis and high lactate concentration in simulated ischemic buffer contribute to the development of reperfusion injury.

• Journal of Ginseng Research
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• v.33 no.4
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• pp.283-293
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• 2009

Ginsenosides, one of the most well-known traditional herbal medicines, are used frequently in Korea for the treatment of cardiovascular symptoms. The effects of ginseng saponin on ischemia-induced isolated rat heart were investigated through analyses of hemodynamic changes including perfusion pressure, aortic flow, coronary flow, and cardiac output. Isolated rat hearts were perfused and then subjected to 30 min of global ischemia followed by 60 min of reperfusion with modified Kreb's Henseleit solution. Myocardial contractile function was continuously recorded. Ginseng saponin administered before inducing ischemia significantly prevented decreases in perfusion pressure, aortic flow, coronary flow, and cardiac output. The ginseng saponin administered group significantly recovered all of the hemodynamic parameters, except heart rate, after ischemia-reperfusion (I/R) compared with ischemia control. The intracellular calcium ($[Ca^{2+}]_i$) content in rat neonatal cardiomyocytes was quantitatively determined. Administration of ginseng saponin significantly prevented $[Ca^{2+}]_i$ increase that had been induced by simulated I/R in vitro (p<0.01) in a dose-dependent manner, suggesting that the cardioprotection of ginseng saponin is mediated by the inhibition of $[Ca^{2+}]_i$ increase. Overall, we found that the administration of ginseng saponin has cardioprotective effects on the isolated rat heart after I/R injury. These results indicate that ginseng saponin has distinct cardioprotective effects in an I/R-induced rat heart.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2021.04a
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• pp.57-57
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• 2021

Oxygen glucose deprivation/re-oxygenation (OGD/R) induces neuronal injury via mechanisms that are believed to mimic the pathways associated with brain ischemia. Stachys sieboldii Miq. (Chinese artichoke), which has been extensively used in oriental traditional medicine to treat of ischemic stroke; however, the role of S. sieboldii Miq. (SSM) in OGD/R induced neuronal injury is not yet fully understood. The present research is aimed to investigate the protective effect and possible mechanisms of SSM extract treatment in an in vitro model of OGD/R to simulate ischemia/reperfusion Injury. Pretreatment of these cells with SSM significantly attenuated OGD/R-induced production of reactive oxygen species (ROS) by increasing GPx, SOD, and decreasing MDA. SSM decreased mitochondrial damage caused by OGD/R injury and inhibited the release of cyt-c from mitochondrion to cytoplasm in SH-SY5Y cells. Furthermore, neuronal cell apoptosis caused by OGD/R injury was inhibited by SSM, and SSM could decrease apoptosis by increasing ratio of Bcl-2/Bax and inhibiting caspase signaling pathway in SH-SY5Y cells. SSM demonstrated a neuroprotective effect on the simulated cerebral ischemia in vitro model, and this effect was the inhibition of mitochondria-mediated apoptosis pathway by scavenging of ROS generation. Therefore, SSM may be a promising neuroprotective strategy against ischemic stroke.