• The Journal of Internal Korean Medicine
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• v.25 no.2
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• pp.277-287
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• 2004

Objective : Diabetes is a disease in which the body does not produce or properly use insulin. Etiological studies of diabetes and its complications showed that oxidative stress might playa major role. Therefore, many efforts have been made to regulate oxygen free radicals for treating diabetes and its complications. Because Jindangwon has been known to be effective in treatment of diabetes, the methanol extract of Jindangwon was tested for its effectiveness in reducing the oxidative stress induced by Streptozotocin. Methods : Jindangwon was washed, dried in the shade and crushed. The crushed Jindangwon was extracted 3 times, each time with 3 volumes of methyl alcohol at $60^{\circ}C$ for 24 hours. The extract was filtered and evaporated under reduced pressure using a rotary evaporator to yield 30.6 g. Jindangwon extract was oral-administered to the diabetic rats induced by streptozotocin 50 mg per 1 kg of body weight for 15 days. The efficacy of the Jindangwon extract was examined with regard to the enzymatic pathways involved in the oxygen free radical production and the glutathione balance. Results : he effects of the methanol extract of Jindangwon in streptozotocin-induced diabetics rats with regard to body weight, blood glucose level, hepatic lipid peroxide level, hepatic xanthine oxidase activity and type conversion rate, hepatic glutathione level, hepatic glutathione peroxidase activity, hepatic glutathione reductase activity, hepatic aldose reductase activity, and hepatic sorbitol dehydrogenase activity were favorable enough to suggest that it is a cure for diabetes and its complications. Conclusions :These results support Jindangwon as an effective reducing agent for oxidative stress in the tissues and organs by regulating the production of oxygen free radicals. Jindangwon, in particular, shows promising results for its use as a cure, or preventative medicine for diabetes and its complications by reducing oxidative stress in beta-cells of the pancreas.

• The Journal of Korean Medicine
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• v.27 no.1 s.65
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• pp.91-103
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• 2006

Objectives : Etiological studies of diabetes and its complications showed that oxidative stress might play a major role. Therefore, many effects have been fried to regulate oxygen free radicals for treating diabetes and its complications. Because Holotrichia has been known to be effective for the treatment of diabetes, the methanol extract of Holotrichia was tested for its effectiveness in reducing the oxidative stress induced by streptozotocin. Methods : Holotrichia was washed, dried in the shade and crushed. The crushed Holotrichia was extracted 3 times, each time with 3 volumes of methyl alcohol at $60^{\circ}C$ for 24h. The extract was filtered and evaporated under a reduced pressure using a rotary evaporator to yield 17 g. Holotrichia extract was oral-administed to the diabetic rats induced by streptozotocin 50 mg per 1 kg of body weight for 20 days. The efficacy of the Holotrichia extract was examined with regard to the enzymatic pathways involved in the oxygen free radical production and the glutathione balance. Results : The Effects of the methanol extract of Holotrichia in streptozotocin-induced diabolic rats with regards to body weight, blood glucose level, hepatic lipid peroxide level, hepatic superoxide anion radical content. hepatic xanthine oxidase activity and type conversion rate, hepatic glutathione level, hepatic aldose reductase activity, and hepatic sorbitol dehydrogenase activity were shown to be good enough to cure and prevent the diabetes and its complications. Conclusions : These results indicated that Holotrichia might reduce the oxidative stress in the tissues and organs by regulating the production of oxygen free radicals. Especially, Holotrichia might prevent and cure the diabetes and its complications by reducing the oxidative stress in the ${\beta}$-cells of pancreas. Some suggestions on biophoton experiments were made.

• The Journal of Internal Korean Medicine
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• v.27 no.4
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• pp.811-821
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• 2006

Objectives : Diabetes is a disease in which the body does not produce or properly use insulin. Etiological studies of diabetes and its complications showed that oxidative stress might play a major role. Therefore, many methods have been tried to regulate oxygen free radicals for treating diabetes and its complications. Because Mori foliumhas been known to be effective for the treatment of diabetes, the methanol extract of Mori folium was tested for its effectiveness in reducing the oxidative stress induced by streptozotocin. Methods : The crushed Mori folium was extracted 3 times, each time with 3 volumes of methyl alcohol at $60^{\circ}C$ or 24 h. The extract was filtered and evaporated under reduced pressure using a rotary evaporator to yield 11.7 g. Mori folium extract was oral-administered to diabetic rats induced by streptozotocin at 100 mg per 1 kg of body weight for 20 days. The efficacy of the Mori foliumextract was examined with regard to the enzymatic pathways involved in oxygen free radical production and glutathione balance. Results : The effects of the Mori foliumin streptozotocin-induced diabetic rats with regards to body weight, blood glucose and insulin level, hepatic lipid peroxide level, hepatic glutathione level, hepatic glutathione S-transferase and glutathione peroxidase level, hepatic aldose reductase activity, and hepatic sorbitol dehydrogenase activity were shown to be good enough to cure and prevent diabetes and its complications. Conclusions : These results indicated that Mori folium might reduce oxidative stress in tissues and organs by regulating the production of oxygen free radicals. Especially Mori folium might prevent and cure diabetes and its complications by reducing oxidative stress in the ${\beta}-cells$ of the pancreas.

• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.201-209
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• 1996

Restoration of the blood flow after a period of ischemia is accompanied by generation of toxic oxygen radicals. This phenomenon may account for the occurrence of reperfusion-mediated tissue injury in ischemic hearts. In in vitro studies, although oxygen radicals can be generated from a variety of sources, including xanthine oxidase system, activated leucocytes, mitochondria and others, the most important source and mechanism of oxygen radical production in the post-ischemic reperfused hearts is unclear. In the present study, we tested the hypothesis that the respiratory chain of mitochondria might be an important source of oxygen radicals which are responsible for the development of the reperfusion injury of ischemic hearts. Langendorff-perfused, isolated rat hearts were subjected to 30 min of global ischemia at $37^{\circ}C$, followed by reperfusion. Amytal, a reversible inhibitor of mitochondrial respiration, was employed to assess the mitochondrial contributions to the development of the reperfusion injury. Intact mitochonria were isolated from the control and the post-ischemic reperfused hearts. Mitochondrial oxygen radical generation was measured by chemiluminescence method and the oxidative tissue damage was estimated by measuring a lipid peroxidation product, malondialdehyde(MDA). To evaluate the extent of the reperfusion injury, post-ischemic functional recovery and lactate dehydrogenase(LDH) release were assessed and compared in Amytal-treated and -untreated hearts. Upon reperfusion of the ischemic hearts, MDA release into the coronary effluent was markedly increased. MDA content of mitochondria isolated from the post-ischemic reperfused hearts was increased to 152% of preischemic value, whereas minimal change was observed in extramitochondrial fraction. The generation of superoxide anion was increased about twice in mitochondria from the reperfused hearts than in those from the control hearts. Amytal inhibited the mitochondrial superoxide generation significantly and also suppressed MDA production in the reperfused hearts. Additionally, Amytal prevented the contractile dysfunction and the increased release of LDH observed in the reperfused hearts. In conclusion, these results indicate that the respiratory chain of mitochondria may be an important source of oxygen radical formation in post-ischemic reperfused hearts, and that oxygen radicals originating from the mitochondria may contribute to the development of myocardial reperfusion injury.

• Molecules and Cells
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• v.40 no.11
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• pp.837-846
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• 2017

As a component of the neurovascular unit, cerebral smooth muscle cells (CSMCs) are an important mediator in the development of cerebral vascular diseases such as stroke. Epoxyeicosatrienoic acids (EETs) are the products of arachidonic acid catalyzed by cytochrome P450 epoxygenase. EETs are shown to exert neuroprotective effects. In this article, the role of EET in the growth and apoptosis of CSMCs and the underlying mechanisms under oxygen glucose deprivation (OGD) conditions were addressed. The viability of CMSCs was decreased significantly in the OGD group, while different subtypes of EETs, especially 14,15-EET, could increase the viability of CSMCs under OGD conditions. RAPA (serine/threonine kinase Mammalian Target of Rapamycin), a specific mTOR inhibitor, could elevate the level of oxygen free radicals in CSMCs as well as the anti-apoptotic effects of 14,15-EET under OGD conditions. However, SP600125, a specific JNK (c-Jun N-terminal protein kinase) pathway inhibitor, could attenuate oxygen free radicals levels in CSMCs as well as the anti-apoptotic effects of 14,15-EET under OGD conditions. These results strongly suggest that EETs exert protective functions during the growth and apoptosis of CSMCs, via the JNK/c-Jun and mTOR signaling pathways in vitro. We are the first to disclose the beneficial roles and underlying mechanism of 14,15-EET in CSMC under OGD conditions.

• Natural Product Sciences
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• v.9 no.2
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• pp.80-82
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• 2003

Since reactive oxygen radicals play an important role in carcinogenesis and other human diseases including neurodegenerative states, antioxidants present in natural products have received considerable attention for alleviation of these disease states. Therefore, in order io identify antioxidants in plant extracts, fifty-seven methanolic extracts derided from indigenous Korean plants were primarily assessed for potential to scavenge stable 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radicals. As a result, nine plant extracts were found to exhibit the DPPH free radical scavenging activity in the criteria of $IC_{50}<40\;{\mu}g/ml$. In particular, the extracts of Melioma oldhami $(IC_{50}=0.1\;{\mu}g/ml)$, Myrica rubra $(IC_{50}=16.2\;{\mu}g/ml)$, Sympolocos paniculata $(IC_{50}=23.0\;{\mu}g/ml)$, Carpinus laxiflora $(IC_{50}=25.1\;{\mu}g/ml)$, and Cleyera japonica $(IC_{50}=26.2\;{\mu}g/ml)$ showed a potent radical scavenging activity. Further study for the identification of active compounds from these lead extracts might be warranted.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.2
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• pp.217-223
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• 1998

Oxygen-derived free radicals have been implicated in many important functions in the biological system. Electrical field stimulation (EFS) causes arterial relaxation in animal models. We found that EFS applied to neither muscle nor nerve but to Krebs solution caused a relaxation of rat aorta that had been contracted with phenylephrine. In the present study, therefore, we investigated the characteristics of this EIRF (electrolysis-induced relaxing factor) using rat isolated aorta. Results indicated that EIRF acts irrespective of the presence of endothelium. EIRF shows positive Griess reaction and is diffusible and quite stable. EIRF-induced relaxation was stronger on PE-contracted aorta than on KCl-contracted one, and inhibited by the pretreatment with methylene blue. Zaprinast, a cGMP-specific phosphodiesterase inhibitor, potentiated the EIRF-induced relaxation. $N^G-nitro-L-arginine$, NO synthase inhibitor, did not inhibit the EIRF-induced relaxation. Deferroxamine, but not ascorbic acid, DMSO potentiated the EIRF-induced relaxation. These results indicate that electrolysis of Krebs solution produces a factor that relaxes vascular smooth muscle via cGMP-mediated mechanism.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.427-433
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• 1998

In brain hypoxic-ischemia, an excess release of glutamate and a marked production of reactive oxygen species (ROS) occur in neuronal and non-neuronal cells. The present study investigated the effect of the biological antioxidants dihydrolipoic acid (DHLA) and lipoic acid (LA) on N-methyl-D-aspartate (NMDA)- and ROS-induced neurotoxicity in cultured rat cortical neurons. DHLA enhanced NMDA-evoked rises in intracellular calcium concentration ($[Ca^{2+}]_i$). In contrast, LA did not alter the NMDA-evoked calcium responses but decreased after a brief treatment of dithiothreitol (DTT), which possesses a strong reducing potential. Despite the modulation of NMDA receptor-mediated rises in $[Ca^{2+}]_i$, neither DHLA nor LA altered the NMDA receptor-mediated neurotoxicity, as assessed by measuring the amount of lactate dehydrogenase released from dead or injured cells. DHLA, but not LA, prevented the neurotoxicity induced by xanthine/xanthine oxidase-generated superoxide radicals. Both DHLA and LA decreased the glutathione depletion-induced neurotoxicity. The present data may indicate that biological antioxidants DHLA and LA protect neurons from ischemic injuries via scavenging oxygen free radicals rather than modulating the redox modulatory site(s) of NMDA receptor.

• Advances in Traditional Medicine
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• v.8 no.3
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• pp.266-278
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• 2008

Erythrina stricta, a deciduous tree widely used traditionally in indigenous system of medicine for various ailments such as rheumatism, fever, leprosy, epilepsy etc. The leaves of Erythrina stricta was extracted with ethanol (70%) and used for the evaluation of various in vitro antioxidant assays which includes H - donor activity, nitric oxide scavenging, superoxide anion scavenging, reducing ability, hydroxyl radical, hydrogen peroxide scavenging, total phenolic content, total flavonoid content, total antioxidant activity by thiocyanate and phosphomolybdenum method, metal chelating, $\beta$-carotene bleaching, total peroxy radical assays. The pro-oxidant activity was measured using bleomycin-dependent DNA damage. Ex vivo models like lipid peroxidation and erythrocyte haemolysis were also used to study the antioxidant property of the extract. The various antioxidant activities were compared with suitable standard antioxidants such as ascorbic acid, butylated hydroxyl toluene, $\alpha$-tocopherol, curcumin, quercetin and Trolox. The generation of free radicals viz. $O_2^{{\cdot}-}$, $OH^{\cdot}$, $H_2O_2$, $NO^{\cdot}$ and peroxyl radicals were effectively scavenged by the ethanolic extract of Erythrina stricta. In all the methods, the extract offered strong antioxidant activity in a concentration dependent manner. The total phenolic content, flavonoid content and total antioxidant activity in Erythrina stricta were determined as microgram (g) pyrocatechol, quercetin and $\alpha$-tocopherol equivalent/mg respectively. The extract did not exhibit any prooxidant activity when compared with ascorbic acid. The results obtained in the present study clearly indicates that Erythrina stricta scavenges free radicals and reduces lipid peroxidation, ameliorating the damage imposed by oxidative stress in different disease conditions and serve as a potential source of natural antioxidant.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.5
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• pp.1349-1355
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• 2005

The steamed root of Rehmannia glutinosa has been used for treatment of inner ear diseases, such as tinnitus and hearing loss in traditional Oriental Medicine. In the present study, we investigated the effect of ethanol extract of steamed root R. glutinosa (SRG) on cisplatin cytotoxicity of HEI-OC1 auditory cells. In addition, to investigate the mechanism of SRG on cisplatin cytotoxicity, the effects of SRG on lipid peroxidation as well as scavenging activities against various free radicals were measured in cisplatin-treated cells. Treatment of SRG protected cells from cisplatin and reduced lipid peroxidation in a dose-dependent manner. Furthermore, SRG demonstrated significant scavenging activity against various free radicals, including superoxide radical, hydroxyl radical, hydrogen peroxide, and DPPH radical. These results indicate that SRG protects cisplatin-induced damages of HEI-OC1 cells through inhibition of lipid peroxidation and augmenting scavenging activities against free radials.