• 대한약침학회지
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• 제10권2호통권23호
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• pp.25-30
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• 2007

Objectives : Free radical metabolism seems to occupy a remarkably common position in the mechanisms of aging and aging related disease. Oxidative damage to DNA, lipids. proteins and other molecules may contribute to the development of cancer, cardiovascular disease and possibly neurodegenerative disease. This study was designed to find out whether Carthami Flos Herbal-Acupuncture Solution can scavenge Nitric Oxide(NO) or not. SNAP is NO generator. NO concentration was estimated after 2,6, 12 and 24 hrs in no treatment group, after treatment with Vit. C or 1, 10, 100${\mu}$g/m1 of Carthami Flos Herbal-Acupuncture Solution. There was no significant scavenging effect of Carthami Flos Herbal-Acupuncture Solutionon NO after 2 hrs. But there was a significant scavenging effect of Cafhami Flos Herbal-Acupuncture Solution on NO in 10${\mu}$/m1 group after 6hrs. And there was a significant scavenging effect of carthami Flos Herbal-Acupuncture Solution on NO in 1, 10${\mu}$g/ml group after 12, 24 hrs. These results suggest that Carhami Flos Herbal-Acupuncture Solution has scavenging effect on NO. This study shows that Carthami Flos Herbal-Acupuncture Solution can be used for aging related disease and further studies are required to investigate the antioxidative effects of it.

• The Korean Journal of Physiology and Pharmacology
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• 제24권5호
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• pp.403-412
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• 2020

Diabetic nephropathy (DN) is a hyperglycemia-induced progressive development of renal insufficiency. Excessive glucose can increase mitochondrial reactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction. Our previous study indicated that cilostazol (CTZ) can reduce ROS levels and decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes. This study investigated the potential mechanisms of CTZ in rats with DN and in high glucose-treated mesangial cells. Male Sprague-Dawley rats were fed 5 mg/kg/day of CTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealed that CTZ reduced the thickness of the glomerular basement membrane and improved mitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatment reduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemia and interacted with the intrinsic pathway for regulating cell apoptosis as an antiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROS production, altered the apoptotic status, and down-regulated transforming growth factor beta (TGF-β) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB). Base on the results of our previous and current studies, CTZ deceleration of hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenance of the mitochondrial function and reduction in TGF-β and NF-κB levels.

• Natural Product Sciences
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• 제18권3호
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• pp.177-182
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• 2012

Oxidative stress potentially induces neurotoxicity which is believed to underlie several major age-related diseases of the central nervous system. This study sought to identify the cytoprotective effects of sixty-nine Cambodian plants against glutamate-induced cell death. Cultured HT22 cells were applied as an in vitro model, and neurotoxicity was induced in these neuronal cells by exposure to a determined concentration of glutamate. Sixty-nine plant sources, as Cambodia's indigenous species, were purchased from O'reusey Market, Phnom Penh, and extracted with ethanol. These extracts were screened for cytoprotective effects against glutamate-triggered neurotoxicity in HT22 cells at concentrations of 100 and 300 ${\mu}g/ml$. Of these, eight ethanol extracts, bark of Anacardium occidentale, bark and sapwood of Bauhinia pulla, flowers of Borassus flabellifer, stems and leaves of Coix lacryma-jobi, bark and sapwood of Diospyros nitida, sapwood of Dipterocarpus obtusifolius, stems of Oryza rufipogon, and fruits of Phyllanthus emblica, showed significant cytoprotective effects against glutamate-induced cell damage and degeneration in HT22 cells.

• 생약학회지
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• 제34권3호통권134호
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• pp.242-245
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• 2003

The effects of chelidonine, a benzophenanthridine isoquinoline alkaloid, on L-DOPA-induced cytotoxicity in PC12 cells were investigated. The treatment of PC12 cells with chelidonine $(1-4\;{\mu}M)$ decreased dopamine content in a dose-dependent manner (30.2% inhibition at $4\;{\mu}M)$. Chelidonine was not cytotoxic up to $4\;{\mu}M)$. However, chelidonine at concentrations higher than $5\;{\mu}M$ caused a cytotoxicity in PC12 cells. L-DOPA at concentrations higher than $50\;{\mu}M$ led to cell damage by oxidative stress in PC12 cells. Chelidonine at non-cytotoxic concentration ranges of $1-4{\mu}M$ aggravated L- DOPA $(20-50\;{\mu}M)$-induced cytotoxicity in PC12 cells. The L-DOPA-induced cytotocxicity was synergistically stimulated by chelidonine at concentrations grader than $5\;{\mu}M$. These data demonstrate that chelidonine exacerbates L-DOPA-induced cytotoxicity. Therefore, it is proposed that the long-term L-DOPA therapeutic patients with chelidonine may need to be checked for the adverse symptoms.

• 동의생리병리학회지
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• 제20권6호
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• pp.1459-1466
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• 2006

The water extract of Hwansodan has been traditionally used for treatment of ischemic brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of Hwansodan rescues cells from neurodegenerative disease. PC12 pheochromocytoma cells have been used extensively as a model for studying the cellular and molecular mechanisms of neuronal cell damages. Under deprivation of growth factor and ischemic injury, PC12 cells spontaneously undergoes apoptotic cell death. Serum and glucose deprivation markedly decreased the viability of PC12 cells, which was characterized with apparent apoptotic features such as membrane blebbing as well as fragmentation of genomic DNA and nuclei. However, the aqueous extract of Hwansodan significantly reduced serum and glucose deprivation-induced cell death and apoptotic characteristics through reduction of intracellular peroxide generation. Pretreatment of Hwansodan also ingibited the activation of caspase-3, in turn, degradation of ICAD/DFF45 was completely abolished in serum and glucose deprivated cells. Furthermore, pretreatment of Hwansodan obviously increased heme oxygenase 1 (HO-1) expression in PC12 cells. Taken together, the data suggest that the protective effects of Hwansodan against serum and glucose deprivation induced oxidative injuries may be achieved through the scavenging of reactive oxygene species accompanying with HO-1 induction.

• 동의생리병리학회지
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• 제20권1호
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• pp.149-155
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• 2006

To prevent human body injury from oxidative stress, antioxidants are very important and many research about antioxidants are generally being conducted. Hydrogen peroxide($H_2O_2$) that is one of vitality oxygen species has been seen that cause various diseases, DNA damage and gene change. The purpose of this study was to examine the inhibition effect of Zizania latifolia Rhizoma on apoptosis induced by $H_2O_2$ in Neuro2A cell. Neuro2A cells were cultivated in RPMI(GibcoBRL) with 5% FBS and treated with $H_2O_2$ and Zizania latifolia Rhizoma. We measured the cell viability and analyzed DNA fragmentation. Activity of PARP, Cytochrome C, caspase-9, caspase-3, p53, p21, Bax and Bcl-2 in the cell was examined dy using western blot. The results obtained were as Follows: The cell viability in Zizania latifolia Rhizoma treatment (60ug/ml<) decreased significantly compared with that of none treatment. (P<0.001) Zizania latifolia Rhizoma increased cell viability about twice as much as that being injury by $H_2O_2$. (Zizania Latifolia Rhizoma 20ug/ml, $H_2O_2$ 200uM, P<0.001) DNA fragmentation developed by $H_2O_2$, but was not developed in Zizania latifolia Rhizoma treatment. PARP, Cytochrome C, caspase-9 and caspase-3 activated all by $H_2O_2$ but were not activated in Zizania latifolia Rhizoma treatment. P53, P2l and Bax activated dy $H_2O_2$, and Bcl-2 got into inactivation. But the opposite results appeared in Zizania latifolia Rhizoma treatment. In conclusion, these results suggest that Zizania latifolia Rhizoma inhibit the development of DNA fragmentation and apoptosis by $H_2O_2$ and the antioxidant action of Zizania latifolia Rhizoma is effective. More researches about effect of Zizania latifolia Rhizoma are considered to need.

• Toxicological Research
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• 제30권4호
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• pp.267-276
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• 2014

Exposures to lead (Pb) are associated with neurological problems including psychiatric disorders and impaired learning and memory. Pb can be absorbed by iron transporters, which are up-regulated in hereditary hemochromatosis, an iron overload disorder in which increased iron deposition in various parenchymal organs promote metal-induced oxidative damage. While dysfunction in HFE (High Fe) gene is the major cause of hemochromatosis, the transport and toxicity of Pb in Hfe-related hemochromatosis are largely unknown. To elucidate the relationship between HFE gene dysfunction and Pb absorption, H67D knock-in Hfe-mutant and wild-type mice were given drinking water containing Pb 1.6 mg/ml ad libitum for 6 weeks and examined for behavioral phenotypes using the nestlet-shredding and marble-burying tests. Latency to nestlet-shredding in Pb-treated wild-type mice was prolonged compared with non-exposed wild-types (p < 0.001), whereas Pb exposure did not alter shredding latency in Hfe-mutant mice. In the marble-burying test, Hfe-mutant mice showed an increased number of marbles buried compared with wild-type mice (p = 0.002), indicating more repetitive behavior upon Hfe mutation. Importantly, Pb-exposed wild-type mice buried more marbles than non-exposed wild-types, whereas the number of marbles buried by Hfe-mutant mice did not change whether or not exposed to Pb. These results suggest that Hfe mutation could normalize Pb-induced behavioral alteration. To explore the mechanism of repetitive behavior caused by Pb, western blot analysis was conducted for proteins involved in brain dopamine metabolism. The levels of tyrosine hydroxylase and dopamine transporter increased upon Pb exposure in both genotypes, whereas Hfe-mutant mice displayed down-regulation of the dopamine transporter and dopamine D1 receptor with D2 receptor elevated. Taken together, our data support the idea that both Pb exposure and Hfe mutation increase repetitive behavior in mice and further suggest that these behavioral changes could be associated with altered dopaminergic neurotransmission, providing a therapeutic basis for psychiatric disorders caused by Pb toxicity.

• Biomolecules & Therapeutics
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• 제20권4호
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• pp.357-370
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• 2012

Radiation therapy, the most commonly used for the treatment of brain tumors, has been shown to be of major significance in tumor control and survival rate of brain tumor patients. About 200,000 patients with brain tumor are treated with either partial large field or whole brain radiation every year in the United States. The use of radiation therapy for treatment of brain tumors, however, may lead to devastating functional deficits in brain several months to years after treatment. In particular, whole brain radiation therapy results in a significant reduction in learning and memory in brain tumor patients as long-term consequences of treatment. Although a number of in vitro and in vivo studies have demonstrated the pathogenesis of radiation-mediated brain injury, the cellular and molecular mechanisms by which radiation induces damage to normal tissue in brain remain largely unknown. Therefore, this review focuses on the pathophysiological mechanisms of whole brain radiation-induced cognitive impairment and the identification of novel therapeutic targets. Specifically, we review the current knowledge about the effects of whole brain radiation on pro-oxidative and pro-inflammatory pathways, matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinases (TIMPs) system and extracellular matrix (ECM), and physiological angiogenesis in brain. These studies may provide a foundation for defining a new cellular and molecular basis related to the etiology of cognitive impairment that occurs among patients in response to whole brain radiation therapy. It may also lead to new opportunities for therapeutic interventions for brain tumor patients who are undergoing whole brain radiation therapy.

• Journal of Plant Biotechnology
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• 제41권4호
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• pp.169-179
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• 2014

세포내에는 비효소적 반응으로 활성산소류를 제거하는 소분자의 항산화 물질과 과산소와 하이드로페록사이드를 분해하는 효소들이 존재한다. 항산화 시스템은 자유라디칼과 활성산소류를 제거함으로써 산화스트레스로부터 세포 구성요소들을 보호하는 역할을 한다. 비효소적 항산화 물질은 지용성과 친수성이 있는데, 지용성 물질들은 세포막에 위치하며 과산화지질이 형성되는 반응을 억제한다. 카로테노이드와 비타민E, $CoQ_{10}$은 세포 내에서 주요 지용성 항산화 물질로써, 이들이 대량으로 축적된 주요 작물의 개발은 영양학적 가치가 높은 식품을 생산할 수 있다. 본 총설에서는 식물에서 카로테노이드와 비타민E, $CoQ_{10}$의 생합성 경로와 대사공학을 이용한 영양강화 연구 현황을 기술하였다.

• 생명과학회지
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• 제17권12호
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• pp.1634-1640
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• 2007

음나무 (Kalopanax pictus, 이하 KP)의 추출물과 ascorbic acid(AA)의 DPPH와 ABTS 라디칼, FRAP 및 NO 소거능 상승효과를 조사하였다. 라디칼 소거능과 항산화능은 농도에 비례하여 증가하였으며, AA 첨가에 의해서 그 활성이 향상되었다. 인간 간암세포주에 대한 KP추출물+AA의 항암능은 MTT법에서 우수한 효과를 나타내었으며 세포 사멸을 유도하였다. 또한 KP 추출물+AA는 세포주기의 G0/G1-phase 또는 G2/M-phase에 영향을 미쳤으며, 농도 의존적인 효과를 나타내었다. 그리고 KP추출물+AA는 대식세포주를 이용한 NO생성과 억제의 면역활성 영향을 나타내었다. 결론적으로 KP추출물의 항산화, 항암 및 면역조절 효과는 KP추출물 단독으로 처리할 때보다, KP 추출물과 AA를 동시에 처리한 경우가 더욱 효과적이었다.