• 생약학회지
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• 제44권3호
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• pp.269-274
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• 2013

In this study, we investigated the anticancer effect of rice bran extract in HL-60 human promyelocytic leukemia cells. The extract of rice bran inhibited the proliferation of HL-60 cells. When treated with the rice bran extract, we could observe the apoptotic characteristics such as apoptotic bodies and the increase of sub-G1 hypodiploid cell population, increase of Bax level, decrease of Bcl-2 expression, cleavage of procaspase-3, cleavage of procaspase-9 and cleavage of poly(ADP-ribose) polymerase(PARP) in HL-60 cells. Furthermore, the apoptosis induction of HL-60 cells treated with the rice bran extract was also accompanied by the inactivation of mitogen-activated protein kinases (MAPK) such as ERK1/2 MAPK and p38 MAPK. In addition, the rice bran extract induced the down-regulation of c-myc. These data suggested that the rice bran extract could induce the apoptosis via the inactivation of ERK1/2 MAPK and p38 MAPK, and the down-regulation of c-myc in HL-60 acute pomyelocytic leukemia cells. The results support that the rice bran extract might have potential for the treatment of acute promyelocytic leukemia.

• 한국육종학회지
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• 제43권1호
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• pp.1-13
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• 2011

Low temperature stress is one of the major negative factors affecting vegetative and reproductive growth of rice. To better understand responses of rice plants to low temperature we analyzed transcriptome expression patterns in glumous flower of cold-tolerant japonica rice variety, Stejaree45, and cold-susceptible variety, HR19621-AC6 at booting stage under cold water irrigation. A total of 2,411 probes were differentially expressed by low temperature in glumous flowers of the two varieties. Some important genes involved in hormone biosynthesis showed variety-specific regulation. Expression of GA20ox3 and GA2ox, among the genes involved in GA biosynthesis, was regulated differentially in the two varieties. Among the genes involved in IAA biosynthesis, YUCCA1 and TAA1:1 showed variety-specific regulation. Among the genes involved in cytokinin biosynthsis and signaling, expression of LOG, HK1 and HK3 was significantly down-regulated only in the cold-susceptible variety. Among the genes involved in ABA biosynthesis, NSY and AAO3 were down-regulated only in the cold-tolerant variety. In general, genes involved in GA, IAA and cytokinin biosynthesis responded to cold temperature in such a way that capacity of those bioactive hormones is maintained at relatively higher levels under cold temperature in the cold-tolerant variety, which can help minimize cold stress imposed to developing reproductive organs in the cold-tolerant variety.

• 대한의생명과학회지
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• 제26권4호
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• pp.288-295
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• 2020

Infection of Helicobacter pylori on gastric mucosa is associated with various gastric diseases. According to the WHO, H. pylori causes gastric cancer and has been classified as a class I carcinogen. Riboflavin is an essential vitamin which presents in a wide variety of foods. Previous studies have shown that riboflavin/UVA was effective against the growth inhibition of Staphylococcus aureus, S. epidermidis and multidrug-resistant Pseudomonas aeruginosa and had the potential for antimicrobial properties. Thus, we hypothesized that riboflavin has a potential role in the growth inhibition of H. pylori. To demonstrate inhibitory concentration of riboflavin against H. pylori, we performed agar and broth dilution methods. As a result, we found that riboflavin inhibited the growth of H. pylori. The MIC was 1 mM in agar and broth dilution test. Furthermore, to explain the inhibitory mechanism, we investigated whether riboflavin has an influence on the replication-associated molecules of the bacteria using RT-PCR to detect mRNA expression level in H. pylori. Riboflavin treatment of H. pylori led to down-regulation of polA and dnaB mRNA expression levels in a dose dependent manner. After then, we also confirmed whether riboflavin has cytotoxicity to human cells. We used AGS, a gastric cancer cell line, and treated with riboflavin did not show statistically significant decrease of cell viability. Thus, these results indicate that riboflavin can suppress the replication machinery of H. pylori. Taken together, these findings demonstrate that riboflavin inhibits growth of H. pylori by inhibiting replication of the bacteria.

• Biomolecules & Therapeutics
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• 제30권6호
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• pp.540-545
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• 2022

Betulin is a triterpenoid natural product contained in several medicinal plants including Betulae Cortex. These medicinal plants have been used for controlling diverse inflammatory diseases in folk medicine and betulin showed anti-inflammatory, antioxidative, and anticancer activities. In this study, we tried to examine whether betulin exerts a regulative effect on the gene expression of MUC5AC mucin under the status simulating a pulmonary inflammation, in human airway epithelial cells. Confluent NCI-H292 cells were pretreated with betulin for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h or the indicated periods. The MUC5AC mucin mRNA expression and mucin glycoprotein production were measured by reverse transcription - polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. To elucidate the action mechanism of betulin, effect of betulin on PMA-induced nuclear factor kappa B (NF-kB) signaling pathway was also investigated by western blot analysis. The results were as follows: 1) Betulin significantly suppressed the production of MUC5AC mucin glycoprotein and down-regulated MUC5AC mRNA expression induced by PMA in NCI-H292 cells. 2) Betulin inhibited NF-κB activation stimulated by PMA. Suppression of inhibitory kappa B kinase (IKK) by betulin led to the inhibition of the phosphorylation and degradation of inhibitory kappa B alpha (IκBα), and the nuclear translocation of NF-κB p65. This, in turn, led to the down-regulation of MUC5AC glycoprotein production in NCI-H292 cells. These results suggest betulin inhibits the gene expression of mucin through regulation of NF-kB signaling pathway, in human airway epithelial cells.

• 항공우주정책ㆍ법학회지
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• 제32권2호
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• pp.3-31
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• 2017

지난 2017년 10월 12일 영국 고등법원(Royal Courts of Justice)은 항공기 운항지연에 따른 항공사의 보상책임에 관하여 판단하였다. 2건의 사건이 병합된 사안에서 원고인 승객들은 영국 리버풀을 출발하여 아랍에미레이트의 두바이를 경유하여 각각의 목적지인 방콕과 시드니로 가기 위해 피고 항공사와 운송계약을 체결하였다. 사안에서 최종 목적지에 승객이 연착되었는지 여부를 판단함에 있어서 연결편을 포함하는 전체 항공여정이 고려되어야 한다는 원고측의 주장에 대해 피고 항공사는 첫 번째 항공편에 발생한 연착만이 항공사의 책임을 판정하는 고려의 대상이 되어야 한다고 주장하였다. 결국 이러한 다툼은 유럽연합(EU)의 항공소비자 보호에 관한 Regulation (EC) No. 261/2004의 적용범위에 관한 것이었다. 즉, 첫 번째 항공운송은 EU지역의 공항을 이륙한 항공편이었고, 두 번째 항공운송은 EU가 아닌 다른 지역에서 운항되었고 더욱이 해당 운송인이 EU에서 설립된 항공사가 아니므로 환승 이후의 항공운송에 관해서는 Regulation 261의 적용이 배제되므로 규정된 금전보상의무가 인정될 수 없다고 피고 항공사가 주장하였던 것이다. 본 논문은 이와 같이 연결편에 의한 항공운송 계약의 이행에서 발생한 지연에 관한 Regulation 261의 적용범위가 문제되었던 사례와 유럽연합사법법원(Court of Justice of the European Union, CJEU)의 판례를 검토할 목적에서 기술되었다. 해당 사례를 연구하는 것은 우리 국민과 항공사에게 시사하는 바가 적지 않다. 우선 Regulation 261 규정에 따라, EU지역을 출발하는 모든 항공사를 이용하는 승객은 동 규정의 적용대상에 포함되므로 EU를 출발하는 우리 국적사들은 Regulation의 직접 적용을 받게 된다. 비록 지리적인 이유로 유럽을 출발하여 우리나라를 경유해서 타국으로 환승하는 여객이 사안에서 문제가 되었던 중동지역과 비교할 때 절대적으로 많지는 않을 것으로 생각되지만, 해당 규정의 의미와 판례동향은 분명히 참고가 필요할 것으로 본다. 나아가 그 서문에서 천명하고 있는 바와 같이 Regulation 261은 기본적으로 항공운송인 보다 소비자인 여객의 권리보호에 친화적인 판례를 다수 도출하고 있는 바, 우리나라의 항공소비자 보호를 위한 법제연구에도 본 연구는 좋은 참고가 될 수 있을 것으로 본다.

• 대한한방내과학회지
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• 제30권4호
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• pp.674-684
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• 2009

Objectives : In conditions of brain infarction, irreversible axon damage occurs in the central nerve system (CNS), because gliosis becomes a physical and a mechanical barrier to axonal regeneration. Reactive gliosis induced by ischemic injury such as middle cerebral artery occlusion is involved with up-regulation of GFAP and CD81. This study was undertaken to examine the effect of the Gongjin-dan (GJD) on CD81 and GFAP expression and its pathway in the rat brain following middle cerebral artery occlusion (MCAO). Methods : In order to study ischemic injuries on the brain, infarction was induced by MCAO using insertion of a single nylon thread, through the internal carotid artery, into a middle cerebral artery. Cresyl violet staining, cerebral infarction size measurement, immunohistochemistry and microscopic examination were used to detect the expression of CD81 and GFAP and the effect on the infarct size and pyramidal cell death in the brain of the rat with cerebral infarction induced by MCAO. Also, c-Fos and ERK expression were measured to investigate the signaling pathway after GJD administration in MCAO rats. Results : Measuring the size of cerebral infarction induced by MCAO in the rat after injection of GJD showed the size had decreased. GJD administration showed pyramidal cell death protection in the hippocampus in the MCAO rat. GJD administration decreased GF AP expression in the MCAO rat. GJD administration decreased CD81 expression in the MCAO rat. GJD administration induced up-regulation of c-FOS expression compared with MCAO. GJD administration induced down-regulation of ERK expression compared with MCAO. Conclusion : We observed that GJD could suppress the reactive gliosis, which disturbs the axonal regeneration in the brain of a rat with cerebral infarction after MCAO by controlling the expression of CD81 and GFAP. The effect may be modulated by the regulation of c-Fos and ERK. These results suggest that GJD can be a candidate to regenerate CNS injury.

• The Korean Journal of Physiology and Pharmacology
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• 제21권1호
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• pp.1-9
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• 2017

Intestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

• The Korean Journal of Physiology and Pharmacology
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• 제18권2호
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• pp.155-161
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• 2014

Overexpression of amyloid precursor protein with the Swedish mutation causes abnormal hyperphosphorylation of the microtubule-associated protein tau. Hyperphosphorylated isoforms of tau are major components of neurofibrillary tangles, which are histopathological hallmarks of Alzheimer's disease. Protein phosphatase 2A (PP2A), a major tau protein phosphatase, consists of a structural A subunit, catalytic C subunit, and a variety of regulatory B subunits. The B subunits have been reported to modulate function of the PP2A holoenzyme by regulating substrate binding, enzyme activity, and subcellular localization. In the current study, we characterized regulatory B subunit-specific regulation of tau protein phosphorylation. We showed that the PP2A B subunit PPP2R2A mediated dephosphorylation of tau protein at Ser-199, Ser-202/Thr-205, Thr-231, Ser-262, and Ser-422. Down-regulation of PPP2R5D expression decreased tau phosphorylation at Ser-202/Thr-205, Thr-231, and Ser-422, which indicates activation of the tau kinase glycogen synthase kinase 3 beta ($GSK3{\beta}$) by PP2A with PPP2R5D subunit. The level of activating phosphorylation of the $GSK3{\beta}$ kinase Akt at Thr-308 and Ser-473 were both increased by PPP2R5D knockdown. We also characterized B subunit-specific phosphorylation sites in tau using mass spectrometric analysis. Liquid chromatography-mass spectrometry revealed that the phosphorylation status of the tau protein may be affected by PP2A, depending on the specific B subunits. These studies further our understanding of the function of various B subunits in mediating site-specific regulation of tau protein phosphorylation.

• 화약ㆍ발파
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• 제20권4호
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• pp.5-15
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• 2002

발파, 항타와 같은 소원음이 존재하는 건설현장에서의 소음저감대책으로는, 소음원 또는 수음점에 방음벽을 설치하여 전파되는 소음을 차단하는 것이 가장 경제적인 경우가 대부분이다. 이러한 방음벽은 소음설계와 구조설계를 통해 그 규모가 결정되며, 방음벽의 구조적 안전을 보장하기 위해서는 KS F4770에 의한 방음판의 구조적 품질이 보장되어야 한다. 본 논문에서는 이 중 금속재 흡음형 방음벽 관련 규정인 F4770-1 - 2001을 분석하여, 그 문제점을 지적하고, 수정 또는 개선 사항을 제시하였다. 분석결과, 보다 경제적인 방음벽의 설치를 위하여 하중의 세분화와 함께 시험방법의 개선이 필요한 것으로 나타났다. 이와 함께 독일의 방음벽 설계시 사용되는 규정인 ZTV-Lsw 88과 비교, 검토하였으며, 검토 결과, 한국 규정은 독일규정에 비해, 보수적인 것으로 나타났다.

• Natural Product Sciences
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• 제24권1호
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• pp.13-20
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• 2018

Estragole is a naturally occurring phenylpropanoid obtained from essential oils found in a broad diversity of plants. Although the phenylpropanoids show many biological activities, clear regulation of the inflammatory signaling pathways has not yet been determined. Here, we scrutinized the anti-inflammatory effect of estragole. The anti-inflammatory effect of estragole was determined through the inhibitory mechanisms of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), nuclear factor kappa B ($NF-{\kappa}B$), and mitogen-activated protein kinases (MAPK) pathways and the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2)/heme oxygenase (HO)-1 pathways in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Estragole significantly inhibited NO production, iNOS and COX-2 expression as well as LPS-induced $NF-{\kappa}B$ and MAPK activation. Furthermore, estragole suppressed LPS-induced intracellular ROS production but up-regulated the stress response gene HO-1 via the activation of transcription factor Nrf-2. These findings demonstrate that estragole inhibits the LPS-induced expression of inflammatory mediators via the down-regulation of iNOS, COX-2, $NF-{\kappa}B$, and MAPK pathways, as well as the up-regulation of the Nrf-2/HO-1 pathway, indicating that this phenylpropanoid has potential therapeutic and preventive applications in various inflammatory diseases.