• 제목/요약/키워드: corm

검색결과 42건 처리시간 0.025초

친종우 종량에 따른 토란 주요형질 및 수량변이 (The Effect of Mother~Corm Weight on Growth and Yield in Taro , Colocasia antiquorum var. Esculenta ENGL.)

  • 최성규
    • 한국자원식물학회지
    • /
    • 제5권2호
    • /
    • pp.129-137
    • /
    • 1992
  • In order to investigate the Possibility of utilizing corm as a seed corm In taro, the corm classified by the weight was planted on April 20, 1984. The effect of weight of corm (30, 50, 70, 90, 110, 130150r and 170g) on the growth, yield, and quality of taro was compared to those raised from cornel.The corm showed a better emergence rate than cermets regardless of its size. The larger the size ofcorm wasi the more the number of leaves developed, and the fisher the yield was. It was consideredthat the higher yield and better quality of taro was obtained by using larger corm as a mother corm( in the following year) due to the increase in the production of large taros.

  • PDF

Carbon monoxide releasing molecule-2 suppresses stretchactivated atrial natriuretic peptide secretion by activating largeconductance calcium-activated potassium channels

  • Li, Weijian;Lee, Sun Hwa;Kim, Suhn Hee
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제26권2호
    • /
    • pp.125-133
    • /
    • 2022
  • Carbon monoxide (CO) is a known gaseous bioactive substance found across a wide array of body systems. The administration of low concentrations of CO has been found to exert an anti-inflammatory, anti-apoptotic, anti-hypertensive, and vaso-dilatory effect. To date, however, it has remained unknown whether CO influences atrial natriuretic peptide (ANP) secretion. This study explores the effect of CO on ANP secretion and its associated signaling pathway using isolated beating rat atria. Atrial perfusate was collected for 10 min for use as a control, after which high atrial stretch was induced by increasing the height of the outflow catheter. Carbon monoxide releasing molecule-2 (CORM-2; 10, 50, 100 μM) and hemin (HO-1 inducer; 0.1, 1, 50 μM), but not CORM-3 (10, 50, 100 μM), decreased high stretch-induced ANP secretion. However, zinc porphyrin (HO-1 inhibitor) did not affect ANP secretion. The order of potency for the suppression of ANP secretion was found to be hemin > CORM-2 >> CORM-3. The suppression of ANP secretion by CORM-2 was attenuated by pretreatment with 5-hydroxydecanoic acid, paxilline, and 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one, but not by diltiazem, wortmannin, LY-294002, or NG-nitro-L-arginine methyl ester. Hypoxic conditions attenuated the suppressive effect of CORM-2 on ANP secretion. In sum, these results suggest that CORM-2 suppresses ANP secretion via mitochondrial KATP channels and large conductance Ca2+-activated K+ channels.

새섬매자기(Scirpus planiculmis)의 출아특성(出芽特性)과 제초제(除草劑) 스크리닝을 위한 구경(球莖)의 보관방법(保管方法) (Studies on the Sprouting Characteristics of Scirpus planiculmis and Storage Methods of Corm for the Herbicide Screening)

  • 황인택;최정섭;김성은;홍경식;조광연
    • 한국잡초학회지
    • /
    • 제14권4호
    • /
    • pp.252-257
    • /
    • 1994
  • 새섬매자기 방제(防除)실험에 사용할 구경(球莖)의 보관방법(保管方法) 및 출아(出芽) 특성(特性)에 대한 조사결과를 요약(要約)하면 다음과 같다. 1. 새섬매자기 구경표면(球莖表面)의 수분(水分)을 제거(除去)하여 $5^{\circ}C$ 냉장고(冷藏庫)에 보관(保管)하면 연중(年中) 균일(均一)한 상태(狀態)로 구경(球莖)을 보관(保管)할 수 있다. 2. 보관중(保管中)에 출아(出芽)된 구경(球莖)의 유모신장(幼苗伸長)을 억제(抑制)하는데는 NaCl 0.5-1.0% 용액(溶液)이 효과적(效果的)이었다. 3. 새섬매자기 구경(球莖)은 건조(乾燥) 및 냉동(冷凍)에 민감(敏感)한 반응(反應)을 나타내기 때문에 수분감소율(水分減少率)이 15% 이상(以上)이 되면 사용하기 어렵고, 냉동사고(冷凍事故) 발생시(發生時) 구경(球莖)의 사용은 어려울 것으로 보인다. 4. 새섬매자기 구경(球莖)의 출아(出芽)에는 항온(恒溫)보다는 변온(變溫)이 효과적(效果的)이었으며, 적합(適合)한 출아온도(出芽溫度)는 $25-35^{\circ}C$에서의 변온조건(變溫條件)이 이상적(理想的)이라 생각되었다. 5. 새섬매자기 구경(球莖)의 출아시(出芽時) NaCl에 대한 내성(耐性)이 동진벼나 논피보다 강하였다. 6. 구경(球莖)을 분할(分割)하였을 경우 출아(出芽)하지 못하는 분할(分割) 구경(球莖)이 발생(發生)하므로 분할(分割) 구경(球莖)을 실험에 사용하는 것은 바람직하지 않았다.

  • PDF

Carbon monoxide releasing molecule-2 protects mice against acute kidney injury through inhibition of ER stress

  • Uddin, Md Jamal;Pak, Eun Seon;Ha, Hunjoo
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제22권5호
    • /
    • pp.567-575
    • /
    • 2018
  • Acute kidney injury (AKI), which is defined as a rapid decline of renal function, becomes common and recently recognized to be closely intertwined with chronic kidney diseases. Current treatment for AKI is largely supportive, and endoplasmic reticulum (ER) stress has emerged as a novel mediator of AKI. Since carbon monoxide attenuates ER stress, the objective of the present study aimed to determine the protective effect of carbon monoxide releasing molecule-2 (CORM2) on AKI associated with ER stress. Kidney injury was induced after LPS (15 mg/kg) treatment at 12 to 24 h in C57BL/6J mice. Pretreatment of CORM2 (30 mg/kg) effectively prevented LPS-induced oxidative stress and inflammation during AKI in mice. CORM2 treatment also effectively inhibited LPS-induced ER stress in AKI mice. In order to confirm effect of CO on the pathophysiological role of tubular epithelial cells in AKI, we used mProx24 cells. Pretreatment of CORM2 attenuated LPS-induced ER stress, oxidative stress, and inflammation in mProx24 cells. These data suggest that CO therapy may prevent ER stress-mediated AKI.

Carbon Monoxide Ameliorates 6-Hydroxydopamine-Induced Cell Death in C6 Glioma Cells

  • Moon, Hyewon;Jang, Jung-Hee;Jang, Tae Chang;Park, Gyu Hwan
    • Biomolecules & Therapeutics
    • /
    • 제26권2호
    • /
    • pp.175-181
    • /
    • 2018
  • Carbon monoxide (CO) is well-known as toxic gas and intrinsic signaling molecule such as neurotransmitter and blood vessel relaxant. Recently, it has been reported that low concentration of CO exerts therapeutic actions under various pathological conditions including liver failure, heart failure, gastric cancer, and cardiac arrest. However, little has been known about the effect of CO in neurodegenerative diseases like Parkinson's disease (PD). To test whether CO could exert a beneficial action during oxidative cell death in PD, we examined the effects of CO on 6-hydroxydopamine (6-OHDA)-induced cell death in C6 glioma cells. Treatment of CO-releasing molecule-2 (CORM-2) significantly attenuated 6-OHDA-induced apoptotic cell death in a dose-dependent manner. CORM-2 treatment decreased Bax/Bcl2 ratio and caspase-3 activity, which had been increased by 6-OHDA. CORM-2 increased phosphorylation of NF-E2-related factor 2 (Nrf2) which is a transcription factor regulating antioxidant proteins. Subsequently, CORM-2 also increased the expression of heme oxygenase-1 and superoxide dismutases (CuZnSOD and MnSOD), which were antioxidant enzymes regulated by Nrf2. These results suggest that CO released by CORM-2 treatment may have protective effects against oxidative cell death in PD through the potentiation of cellular adaptive survival responses via activation of Nrf2 and upregulation of heme oxygenase-1, leading to increasing antioxidant defense capacity.

Heme oxygenase-1 (HO-1)/carbon monoxide (CO) axis suppresses RANKL-induced osteoclastic differentiation by inhibiting redox-sensitive NF-κB activation

  • Bak, Sun-Uk;Kim, Suji;Hwang, Hae-Jun;Yun, Jung-A;Kim, Wan-Sung;Won, Moo-Ho;Kim, Ji-Yoon;Ha, Kwon-Soo;Kwon, Young-Guen;Kim, Young-Myeong
    • BMB Reports
    • /
    • 제50권2호
    • /
    • pp.103-108
    • /
    • 2017
  • Heme oxygenase (HO-1) catalyzes heme to carbon monoxide (CO), biliverdin/bilirubin, and iron and is known to prevent the pathogenesis of several human diseases. We assessed the beneficial effect of heme degradation products on osteoclastogenesis induced by receptor activator of NF-${\kappa}B$ ligand (RANKL). Treatment of RAW264.7 cells with CORM-2 (a CO donor) and bilirubin, but not with iron, decreased RANKL-induced osteoclastogenesis, with CORM-2 having a more potent anti-osteogenic effect. CORM-2 also inhibited RANKL-induced osteoclastogenesis and osteoclastic resorption activity in marrow-derived macrophages. Treatment with hemin, a HO-1 inducer, strongly inhibited RANKL-induced osteoclastogenesis in wild-type macrophages, but was ineffective in $HO-1^{+/-}$ cells. CORM-2 reduced RANKL-induced NFATc1 expression by inhibiting IKK-dependent NF-${\kappa}B$ activation and reactive oxygen species production. These results suggest that CO potently inhibits RANKL-induced osteoclastogenesis by inhibiting redox-sensitive NF-${\kappa}B$-mediated NFATc1 expression. Our findings indicate that HO-1/CO can act as an anti-resorption agent and reduce bone loss by blocking osteoclast differentiation.

Carbon monoxide activation of delayed rectifier potassium currents of human cardiac fibroblasts through diverse pathways

  • Bae, Hyemi;Kim, Taeho;Lim, Inja
    • The Korean Journal of Physiology and Pharmacology
    • /
    • 제26권1호
    • /
    • pp.25-36
    • /
    • 2022
  • To identify the effect and mechanism of carbon monoxide (CO) on delayed rectifier K+ currents (IK) of human cardiac fibroblasts (HCFs), we used the wholecell mode patch-clamp technique. Application of CO delivered by carbon monoxidereleasing molecule-3 (CORM3) increased the amplitude of outward K+ currents, and diphenyl phosphine oxide-1 (a specific IK blocker) inhibited the currents. CORM3-induced augmentation was blocked by pretreatment with nitric oxide synthase blockers (L-NG-monomethyl arginine citrate and L-NG-nitro arginine methyl ester). Pretreatment with KT5823 (a protein kinas G blocker), 1H-[1,-2,-4] oxadiazolo-[4,-3-a] quinoxalin-1-on (ODQ, a soluble guanylate cyclase blocker), KT5720 (a protein kinase A blocker), and SQ22536 (an adenylate cyclase blocker) blocked the CORM3 stimulating effect on IK. In addition, pretreatment with SB239063 (a p38 mitogen-activated protein kinase [MAPK] blocker) and PD98059 (a p44/42 MAPK blocker) also blocked the CORM3's effect on the currents. When testing the involvement of S-nitrosylation, pretreatment of N-ethylmaleimide (a thiol-alkylating reagent) blocked CO-induced IK activation and DL-dithiothreitol (a reducing agent) reversed this effect. Pretreatment with 5,10,15,20-tetrakis(1-methylpyridinium-4-yl)-21H,23H porphyrin manganese (III) pentachloride and manganese (III) tetrakis (4-benzoic acid) porphyrin chloride (superoxide dismutase mimetics), diphenyleneiodonium chloride (an NADPH oxidase blocker), or allopurinol (a xanthine oxidase blocker) also inhibited CO-induced IK activation. These results suggest that CO enhances IK in HCFs through the nitric oxide, phosphorylation by protein kinase G, protein kinase A, and MAPK, S-nitrosylation and reduction/oxidation (redox) signaling pathways.

Liatris Spicata 구경휴면(球莖休眠)에 관(關)한 연구(硏究) -I. 휴면도입기(休眠導入期) 및 각성기(覺醒期) 구명(究明)과 gibberellin 처리(処理)의 휴면타파효과(休眠打破效果) (Studies on the Dormancy of Liatris spicata Corm -I. Study on the Induction and Awakening of Dormancy and Effect of Gibberellin Treatment on the Breaking of Dormancy)

  • 박인환;서영교;전재기;최상태
    • Current Research on Agriculture and Life Sciences
    • /
    • 제4권
    • /
    • pp.18-21
    • /
    • 1986
  • Liatris spicata 구경(球莖)의 휴면도입기(休眠導入期) 및 휴면각성기(休眠覺醒期)를 조사(調査)함과 동시(同時)에 GA처리(處理)에 의(依)한 휴면타파효과(休眠打破效果)를 조사(調査)한 결과(結果)는 다음과 같다. 1. 맹아율(萌芽率), shooting율(率) 및 발근율(發根率)은 8월(月) 30일(日) 이후(以後) 서서히 저하(低下)되어 11월(月) 14일경(日頃) 가장 낮은 경향(傾向)을 보이다가 이후(以後) 서서히 증가(增加)하여 1월(月) 29일(日) 이후(以後)에는 모두 100%로써 매우 양호(良好)하였다. 2. 출아소요일수(出芽所要日數)에 있어서도 11월(月) 14일(日) 무처리구(無處理區)에 있어서 10.1일(日)로써 가장 길었으며 1월(月) 29일(日) 이후(以後)에는 급격(急激)히 단축(短縮)되었다. 3. 맹아(萌芽) 및 shooting 상태(狀態)를 봐서 대구지방(大邱地方)의 노지(露地)에서 Liatris spicata 구경(球莖)의 휴면도입기(休眠導入期)는 9월(月) 하순경(下旬頃), 휴면기(休眠期)는 11월(月) 중순경(中旬頃), 휴면각성기(休眠覺醒期)는 1월(月) 하(下)~2월(月) 초순경(初旬頃)이라고 사료(思料)된다. 4. 구경(球莖)의 휴면타파효과(休眠打破效果)는 GA 200ppm 1시간(時間) 침지처리(浸漬處理)로 효과(效果)가 인정(認定)되었으며 특히(特)히 휴면(休眠)이 깊을수록 그 효과(效果)는 더욱 증가(增加)되는 경향(傾向)을 보였다.

  • PDF

단핵구세포주 THP-1의 대식세포로의 분화 및 활성화에서 CO의 억제 효과 (Carbon Monoxide Inhibits PMA-induced Differentiation in Human Monocytic THP-1 Cells)

  • 김다솔;이미선;김한솔;이혜윤;김오윤;강예린;손동현;김관회;박영철
    • 생명과학회지
    • /
    • 제27권2호
    • /
    • pp.217-224
    • /
    • 2017
  • Carbon monoxide (CO)는 세포 보호의 기능을 가지는 항산화 효소인 heme oxygenase-1 (HO-1)의 대사산물로 세포성장, 아폽토시스, 염증에 대한 억제 효과를 보이는 것으로 보고가 이어지고 있고, 이에 관련된 연구가 활발히 진행되고 있는 실정이다. 본 연구에서는 CO가 단핵구의 대식세포로의 분화 및 그 활성화 과정에 미치는 영향을 인간 단핵구세포주 THP-1을 이용하여 조사하였다. CO-releasing compound인 CORM-2는 phorbol 12-myristate 13-acetate (PMA)로 자극한 THP-1 세포에서 viability와 증식에는 큰 영향을 주지 않았으나 부착능의 뚜렷한 감소를 보였다. 그리고, CORM-2는 대식세포의 막표면 분화 인자인 CD14, CD11b 및 CD18의 발현과 latex beads를 이용한 포식 기능을 현저히 억제하였다. 다음으로, 배양중인 THP-1 세포를 PMA로 6일 동안 대식세포로 분화시킨 후 inflammatory cytokines의 분비와 포식 기능을 조사하였다. CORM-2의 처리는 lipopolysaccaride (LPS)로 자극한 대식세포로부터 분비되는 IL-6와 $TNF-{\alpha}$의 분비를 감소시켰다. 또한, 분화된 대식세포에 E. coli (K-12 strain) bioparticles를 이용하여 포식 기능을 측정한 결과 CORM-2를 처리한 세포에서는 현저히 감소되는 경향을 보였다. 이를 종합해 볼 때, CO는 항원 인식과 포식 기능에 관여하는 막단백질의 발현을 저해함으로써 단핵구의 분화과정을 억제하였고, 분화된 대식세포의 inflammatory cytokines의 분비 및 포식 기능을 저해함으로써 활성화 과정도 억제하는 것으로 보인다.