• Journal of Microbiology and Biotechnology
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• 제23권2호
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• pp.211-217
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• 2013

Corynebacterium glutamicum is one of the well-studied industrial strain that is used for the production of nucleotides and amino acids. Recently, it has also been studied as a possible producer of organic acids such as succinic acid, based on its ability to produce organic acids under an oxygen deprivation condition. In this study, we conducted the optimization of medium components for improved succinate production from C. glutamicum under an oxygen deprivation condition by Plackett-Burman design and applied a response surface methodology. A Plackett-Burman design for ten factors such as glucose, ammonium sulfate, magnesium sulfate, potassium phosphate ($K_2HPO_4$ and $KH_2PO_4$), iron sulfate, manganese sulfate, biotin, thiamine, and sodium bicarbonate was applied to evaluate the effects on succinate production. Glucose, ammonium sulfate, magnesium sulfate, and dipotassium phosphate were found to have significant influence on succinate production, and the optimal concentrations of these four factors were sequentially investigated by the response surface methodology using a Box-Behnken design. The optimal medium components obtained for achieving maximum concentration of succinic acid were as follows: glucose 10 g/l, magnesium sulfate 0.5 g/l, dipotassium phosphate ($K_2HPO_4$) 0.75 g/l, potassium dihydrogen phosphate ($KH_2PO_4$) 0.5 g/l, iron sulfate 6 mg/l, manganese sulfate 4.2 mg/l, biotin 0.2 mg/l, thiamine 0.2 mg/l, and sodium bicarbonate 100 mM. The parameters that differed from a normal BT medium were glucose changed from 40 g/l to 10 g/l, dipotassium phosphate ($K_2HPO_4$) 0.5 g/l changed to 0.75 g/l, and ammonium sulfate ($(NH_4)_2SO_4$) 7 g/l changed to 0 g/l. Under these conditions, the final succinic acid concentration was 16.3 mM, which is about 1.46 fold higher than the original medium (11.1 mM) at 24 h. This work showed the improvement of succinate production by a simple change of media components deduced from sequential optimization.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.302.2-303
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• 2002

Oxidative stress has been implicated in the pathophysiology of many neurodegenerative disorders including Alzheimer's and Parkinson's diseases. Baicalein. baicalin and wogonin. the major constituents of Scutellaria baicalensis. have been reported to exhibit antioxidant properties in many different bioassay systems. The present study evaluated neuroprotective effects of these flavonoids on various neuronal injuries induced in primary cultured rat cortical cells by oxidative stress. NMDA. oxygen-glucose deprivation. and $A{\beta}$(25-35). (omitted)

• 한국미생물·생명공학회지
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• 제35권4호
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• pp.292-297
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• 2007

H. pluviails는 고광도와 질소 결핍 배지 조건에서 ketocarotenoid의 일종인 astaxanthin을 다량 축적하는 녹조류이다. 스트레스가 없는 조건에서 키운 green cell과 astaxanthin이 합성된 red cell을 HPLC를 통해 비교해 본 결과 각 색소의 양이 변화하는 것을 볼 수 있었다. 여러 ester 형태의 astaxanthin이 생합성 되고, zeaxanthin이 늘어난 반면, lutein과 ${\beta}$-carotene은 감소하였다. 또한 total chlorophyll 양이 줄어드는 대신 total carotenoid의 양이 늘어남을 보였다. H. pluvilalis에서 찾아낸 astaxanthin 생합성 경로에 있는 carotenoid hydroxylase, phytoene desaturase, isopentenyl pyrophosphate isomerase, ${\beta}$-carotene ketolase 유전자는 음성대조군인 chloroplast chlorophyll a-b binding protein와는 달리cell이 성장하기 좋은 조건의 상태보다 astaxanthin을 생합성하기 위해 고광도의 스트레스를 받았을 때 더 높은 발현양상을 보이는 것을 확인할 수 있었다.

• 대한한방내과학회지
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• 제25권3호
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• pp.461-472
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• 2004

Objectives : For the screening of neuroprotective effects of medicinal herbs, the complex system of animal models suffer some disadvantages in controlling critical parameters such as blood pressure and body temperature. Additionally, application of drugs to the appropriate brain area sometimes is difficult, due to poor permeability though the blood brain barrier, and so potential protective effects might be masked. Methods : Organotypic hippocampal slice culture (OHSC) method has the advantages of being relatively easy to prepare and of maintaining the general structure, including tissue integrity and the connections between cells. Drugs can easily be applied and neuronal damage can easily be quantified by using tissues and culture media. This study demonstrates neuroprotective effects of Puerariae radix (葛根, PR), Salviae miltiorrhizae radix (丹蔘, SR), Rhei rhizoma (大黃, RR), and Bupleuri radix (柴胡, BR). These were screenedand compared to MK-801, antagonist of NMDA receptors, by using OHSC of 1 week-old Sprague-Dawley rats. Oxygen/glucose deprivation (OGD) were conducted in an anaerobic chamber $(85%\;N_2,\;10%\;CO_2\;and\;5%\;H_2)$ in a deoxygenated glucose-free medium for 60 minutes. Water extracts of each herbs were treated to culture media with $5\;{\mu}g/ml$ for 48 hours. Results : Neuronal cell death in the cultures was monitored by densitometric measurements of the cellular uptake of propidium iodide (PI). PI fluorescence images were obtained at 48 hours after the OGD and medicinal herb treatment. Also TUNEL-positive cells in the CAI and DG regions and LDH concentrations in culture media were measured at 48 hours after the OGD. According to measured data, MK-801, PR, SR and BR demonstrated significant neuroprotective effect against excessive neuronal cell death and apoptosis induced by the OGD insult. Especially, PR revealed similar neuroprotective effect to MK-801 and RR demonstrated weak neuroprotective effect. Conclusions : These results suggest that OHSC can be a suitable method for screening of neuroprotective effects of medicinal herbs. (This work was supported by the research program of Dongguk University and Grant 01-PJ9-PG1-01CO03-0003 from Ministry of Health & Welfare.)

• The Korean Journal of Physiology and Pharmacology
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• 제18권5호
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• pp.403-409
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• 2014

The Bis protein is known to be involved in a variety of cellular processes including apoptosis, migration, autophagy as well as protein quality control. Bis expression is induced in response to a number of types of stress, such as heat shock or a proteasome inhibitor via the activation of heat shock factor (HSF)1. We report herein that Bis expression is increased at the transcriptional level in HK-2 kidney tubular cells and A172 glioma cells by exposure to oxidative stress such as $H_2O_2$ treatment and oxygen-glucose deprivation, respectively. The pretreatment of HK-2 cells with N-acetyl cysteine, suppressed Bis induction. Furthermore, HSF1 silencing attenuated Bis expression that was induced by $H_2O_2$, accompanied by increase in reactive oxygen species (ROS) accumulation. Using a series of deletion constructs of the bis gene promoter, two putative heat shock elements located in the proximal region of the bis gene promoter were found to be essential for the constitutive expression is as well as the inducible expression of Bis. Taken together, our results indicate that oxidative stress induces Bis expression at the transcriptional levels via activation of HSF1, which might confer an expansion of antioxidant capacity against pro-oxidant milieu. However, the possible role of the other cis-element in the induction of Bis remains to be determined.

• 대한장애인치과학회지
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• 제8권1호
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• pp.22-25
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• 2012

1. 저산소성 허혈성 뇌병변 환아에서 뇌손상으로 인한 혀내밀기 습관에 의해 외상성 혀궤양이 발생할 수 있으며 Riga-Fede disease로 진단할 수 있다. 2. Riga-Fede disease의 종래의 치료 방법은 하악 유전치의 날카로운 부분을 갈아주는 것, 절단면의 복합레진 수복, 발치 등이 있으며 이번 보고에서는 보존적이며 가역적인 방법인 tongue protector를 제안하였고 혀궤양의 치료 및 혀내밀기습관 개선에 효과적인 것으로 나타났다.

• BMB Reports
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• 제52권7호
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• pp.439-444
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• 2019

Although hypoxic/ischemic injury is thought to contribute to the incidence of Alzheimer's disease (AD), the molecular mechanism that determines the relationship between hypoxia-induced ${\beta}$-amyloid ($A{\beta}$) generation and development of AD is not yet known. We have now investigated the protective effects of N,4,5-trimethylthiazol-2-amine hydrochloride (KHG26702), a novel thiazole derivative, on oxygen-glucose deprivation (OGD)-reoxygenation (OGD-R)-induced $A{\beta}$ production in SH-SY5Y human neuroblastoma cells. Pretreatment of these cells with KHG26702 significantly attenuated OGD-R-induced production of reactive oxygen species and elevation of levels of malondialdehyde, prostaglandin $E_2$, interleukin 6 and glutathione, as well as superoxide dismutase activity. KHG26702 also reduced OGD-R-induced expression of the apoptotic protein caspase-3, the apoptosis regulator Bcl-2, and the autophagy protein becn-1. Finally, KHG26702 reduced OGD-R-induced $A{\beta}$ production and cleavage of amyloid precursor protein, by inhibiting secretase activity and suppressing the autophagic pathway. Although supporting data from in vivo studies are required, our results indicate that KHG26702 may prevent neuronal cell damage from OGD-R-induced toxicity.

• Korean Circulation Journal
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• 제53권3호
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• pp.151-167
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• 2023

Background and Objectives: Acute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI. However, the specific mechanism of ferroptosis in AMI remains unclear. Methods: We constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage. Results: AC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI. Conclusions: AC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.

• The Korean Journal of Physiology and Pharmacology
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• 제10권4호
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• pp.173-180
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• 2006

Microglial activation is thought to play a role in the pathogenesis of many brain disorders. Therefore, understanding the response of microglia to noxious stimuli may provide insights into their role in disorders such as stroke and neurodegeneration. Many genes involved in this response have been identified individually, but not systematically. In this regards, the microarray system permitted to screen a large number of genes in biological or pathological processes. Therefore, we used microarray technology to evaluate the effect of oxygen glucose deprivation (OGD) and reperfusion on gene expression in microglia under ischemia-like and activating conditions. Primary microglial cultures were prepared from postnatal mice brain. The cells were exposed to 4 hrs of OGD and 1 h of reperfusion at $37^{\circ}C$. Isolated mRNA were run on GeneChips. After OGD and reperfusion, ＞2-fold increases of 90 genes and ＞2-fold decrease of 41 genes were found. Among the genes differentially increased by OGD and reperfusion in microglia were inflammatory and immune related genes such as prostaglandin E synthase, $IL-1{\beta}$, and $TNF-{\alpha}$. Microarray analysis of gene expression may be useful for elucidating novel molecular mediators of microglial reaction to reperfusion injury and provide insights into the molecular basis of brain disorders.

• Journal of Korean Neurosurgical Society
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• 제60권4호
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• pp.391-396
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• 2017

Objective : To investigate the neuroprotective effects of Ginkgolide B (GB) against ischemic stroke-induced injury in vivo and in vitro, and further explore the possible mechanisms concerned. Methods : Transient middle cerebral artery occlusion (tMCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated N2a cells were used to explore the neuroprotective effects of GB. The expression of brain-derived neurotrophic factor (BDNF) was detected via Western blot and qRT-PCR. Results : GB treatment (4 mg/kg, i. p., bid) significantly reduced neurological deficits, water content, and cerebral infarct volume in tMCAO mice. GB also significantly increased Bcl-2/Bax ratio, reduced the expression of caspase-3, and protected against OGD/R-induced neuronal apoptosis. Meanwhile, GB caused the up-regulation of BDNF protein in vivo and in vitro. Conclusion : Our data suggest that GB might protect the brain against ischemic insult partly via modulating BDNF expression.