• Journal of Animal Science and Technology
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• 제65권4호
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• pp.838-855
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• 2023

The highly pathogenic avian influenza (HPAI) virus triggers infectious diseases, resulting in pulmonary damage and high mortality in domestic poultry worldwide. This study aimed to analyze miRNA expression profiles after infection with the HPAI H5N1 virus in resistant and susceptible lines of Ri chickens.For this purpose, resistant and susceptible lines of Vietnamese Ri chicken were used based on the A/G allele of Mx and BF2 genes. These genes are responsible for innate antiviral activity and were selected to determine differentially expressed (DE) miRNAs in HPAI-infected chicken lines using small RNA sequencing. A total of 44 miRNAs were DE after 3 days of infection with the H5N1 virus. Computational program analysis indicated the candidate target genes for DE miRNAs to possess significant functions related to cytokines, chemokines, MAPK signaling pathway, ErBb signaling pathway, and Wnt signaling pathway. Several DE miRNA-mRNA matches were suggested to play crucial roles in mediating immune functions against viral evasion. These results revealed the potential regulatory roles of miRNAs in the immune response of the two Ri chicken lines against HPAI H5N1 virus infection in the lungs.

• The Korean Journal of Physiology and Pharmacology
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• 제7권6호
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• pp.357-362
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• 2003

Carbon monoxide (CO) is low molecular weight oxide gas that is endogenously produced under physiological conditions and interacts with another gas, nitric oxide (NO), to act as a gastrointestinal messenger. The aim of this study was to determine the effects of exogenous CO on L-type calcium channel currents of human jejunal circular smooth muscle cells. Cells were voltage clamped with 10 mM barium ($Ba^{2+}$) as the charge carrier, and CO was directly applied into the bath to avoid perfusion induced effects on the recorded currents. 0.2% CO was increased barium current ($I_{Ba}$) by $15{\pm}2$% ($mean{\pm}S.E.$, p<0.01, n=11) in the cells. To determine if the effects of CO on barium current were mediated through the cGMP pathway, cells were pretreated with 1-H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ, $10{mu}M$), a soluble guanylyl cyclase inhibitor, and exogenous CO (0.2%) had no effect on barium currents in the presence of ODQ ($2{\pm}1$% increase, n=6, p>0.05). CO mediates inhibitory neurotransmission through the nitric oxide pathway. Therefore, to determine if the effects of CO on L-calcium channels were also mediated through NO, cells were incubated with $N^G-nitro-L-arginine$ (L-NNA, 1 mM), a nitric oxide synthase inhibitor. After L-NNA pretreatment, 0.2 % CO did not increase barium current ($4{\pm}2$% increase, n=6, p>0.05). NO donor, SNAP ($20{\mu}M$) increased barium current by $13{\pm}2$% (n=6, p<0.05) in human jejunal smooth muscle cells. These data suggest that CO activates L-type calcium channels through NO/cGMP dependant mechanism.

• Bulletin of the Korean Chemical Society
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• 제33권2호
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• pp.499-504
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• 2012

The specific rates of sovolysis of 4-methylthiophene-2-carbonyl chloride (1) have been determined in 26 pure and binary solvents at $25.0^{\circ}C$. Product selectivities are reported for solvolyses of 1 in aqueous ethanol and methanol binary mixtures. Comparison of the specific rates of solvolyses of 1 with those for p-methoxybenzoyl chloride (2) in terms of linear free energy relationships (LFER) are helpful in mechanistic considerations, as is also treatment in terms of the extended Grunwald-Winstein equation. It is proposed that the solvolyses of 1 in binary aqueous solvent mixtures proceed through an SN1 and/or ionization (I) pathway rather than through an associative $S_N2$ and/or addition-elimination (A-E) pathway.

• 대한기계학회논문집B
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• 제34권4호
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• pp.365-373
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• 2010

제트 혼합 반응기(JSR) 내의 NOx와 같은 배출물질을 예측하기 위해서 화학반응기 모델을 개발했다. 본 연구에서는 JSR에 대한 화학반응기 모델로서 two-PSR 모델이 채택되었다. CHEMKIN 코드와 4가지 NO 생성 메커니즘을 포함한 GRI 3.0 메탄-공기 연소 메커니즘을 이용해서 JSR내의 희박 예혼합 메탄-공기 연소의 NO 생성예측을 실시하였다. 모델의 검증을 위해서 계산된 결과를 Rutar의 실험 데이터와 비교하였다. NO 생성의 중요 파라미터와 4 가지 NO 경로의 기여도를 조사하였다. 화염 영역에서는 prompt 메커니즘이 주된 경로이고, 화염후영역에서는 Zeldovich 메커니즘이 주된 경로이다. 희박 예혼합 조건에서는 N2O 메카니즘이가 화염 및 화염후 영역 모두에서 중요한 경로이다.

• Bulletin of the Korean Chemical Society
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• 제33권11호
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• pp.3657-3664
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• 2012

Reactions of 1-adamantylmethyl chloroformate ($1-AdCH_2OCOCl$, 1) and 1-adamantylmethyl fluoroformate ($1-AdCH_2OCOF$, 2) in hydroxylic solvents have been studied. Application of the extended Grunwald-Winstein (G-W) equation to solvolyses of 1 in a variety of pure and binary solvents indicates an addition-elimination pathway in the majority of the solvents except an ionization pathway in the solvents of relatively low nucleophilcity and high ionizing power. The solvolyses of 2 show an addition-elimination pathway in all of the mixed solvents. The leaving group effects ($k_F/k_{Cl}$), the kinetic solvent isotope effects (KSIEs, $k_{MeOH}/k_{MeOD}$), and the enthalpy and entropy of activation for the solvolyses of 1 and 2 were also calculated. The selectivity values (S) for each solvent composition are reported and discussed. These observations are compared with those previously reported for other alkyl haloformate esters.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.170.2-170.2
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• 2003

Ras expression has been suggested as a marker for tumor aggressiveness of breast cancer, including the degrees of invasion and tumor recurrence. We previously showed that p38 MAPK is a key signaling molecule differentially regulated by H-ras and N-ras, leading to H-ras-specific cell invasive and migrative phenotypes in human breast epithelial cells (Cancer Res: 63, 5454-5461, 2003). In this study, we further investigated the role of p38 MARK pathway in the induction of metastatic potential in MCF10A cells as a "gain of function" study. (omitted)

• Molecules and Cells
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• 제21권1호
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• pp.42-51
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• 2006

We investigated the mechanism of contraction induced by S1P in esophageal smooth muscle cells. Western blot analysis demonstrated that $S1P_1$, $S1P_2$, $S1P_3$, and $S1P_5$ receptors existed in the cat esophagus. Only penetration of EDG-5 ($S1P_2$) antibody into permeabilized cells inhibited S1P-induced contraction. Pertussis toxin (PTX) also inhibited contraction, suggesting that it was mediated by $S1P_2$ receptors coupled to a PTXsensitive $G_i$ protein. Specific antibodies to $G_{i2}$, $G_q$ and $G_{\beta}$ inhibited contraction, implying that the S1P-induced contraction depends on PTX-insensitive $G_q$ and $G_{\beta}$ dimers as well as the PTX-sensitive $G_{i2}$. Contraction was not affected by the phospholipase $A_2$ inhibitor DEDA, or the PLD inhibitor ${\rho}$-chloromercuribenzoate, but it was abolished by the PLC inhibitor U73122. Incubation of permeabilized cells with $PLC{\beta}3$ antibody also inhibited contraction. Contraction involved the activation of a PKC pathway since it was affected by GF109203X and chelerythrine. Since $PKC{\varepsilon}$ antibody inhibited contraction, $PKC{\varepsilon}$ may be required. Preincubation of the muscle cells with the MEK inhibitor PD98059 blocked S1P-induced contraction, but the p38 MAP kinase inhibitor SB202190 did not. In addition, co-treatment of cells with GF 109203X and PD98059 did not have a synergistic effect, suggesting that these two kinases are involved in the same signaling pathway. Our data suggest that S1P-induced contraction in esophageal smooth muscle cells is mediated by $S1P_2$ receptors coupled to PTX-sensitive $G_{i2}$ proteins, and PTX-insensitive $G_q$ and $G_{\beta}$ proteins, and that the resulting activation of the $PLC{\beta}3$ and $PKC{\varepsilon}$ pathway leads to activation of a p44/p42 MAPK pathway.

• The Korean Journal of Pain
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• 제34권4호
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• pp.405-416
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• 2021

Background: This study investigated the effect of intrathecal Sec-O-glucosylhamaudol (SOG) on the p38/c-Jun N-terminal kinase (JNK) signaling pathways, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-related inflammatory responses, and autophagy in a spinal nerve ligation (SNL)-induced neuropathic pain model. Methods: The continuous administration of intrathecal SOG via an osmotic pump was performed on male Sprague-Dawley rats (n = 50) with SNL-induced neuropathic pain. Rats were randomized into four groups after the 7th day following SNL and treated for 2 weeks as follows (each n = 10): Group S, sham-operated; Group D, 70% dimethylsulfoxide; Group SOG96, SOG at 96 ㎍/day; and Group SOG192, SOG at 192 ㎍/day. The paw withdrawal threshold (PWT) test was performed to assess neuropathic pain. Western blotting of the spinal cord (L5) was performed to measure changes in the expression of signaling pathway components, cytokines, and autophagy. Additional studies with naloxone challenge (n = 10) and cells were carried out to evaluate the potential mechanisms underlying the effects of SOG. Results: Continuous intrathecal SOG administration increased the PWT with p38/JNK mitogen-activated protein kinase (MAPK) pathway and NF-κB signaling pathway inhibition, which induced a reduction in proinflammatory cytokines with the concomitant downregulation of autophagy. Conclusions: SOG alleviates mechanical allodynia, and its mechanism is thought to be related to the regulation of p38/JNK MAPK and NF-κB signaling pathways, associated with autophagy during neuroinflammatory processes after SNL.

• Journal of Yeungnam Medical Science
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• 제14권2호
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• pp.337-349
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• 1997

세균 내독소에 의하여 발생하는 패혈성 쇼크와 혈관 반응성 감소의 원인을 관찰하였다. 혈관 절편이 고정된 실험조에 세균 내독소 0.2 mg 투여한 경우 $36{\pm}3.65$ nM NO가 발생되었고, NO 발생에 의한 혈관 이완 효과를 억제하기 위해 전처치한 L-MAME, methylene blue는 혈관 절편의 phenylephrine (PE) 유발 수축 반응을 증가시켰으며 methylene blue에 의해 더 강한 수축 반응의 증가가 관찰되었다. 이때 혈관 내피세포가 존재할 경우에 PE에 대한 혈관 반응성이 증가되는 경향을 나타내었다. 세균 내독소 투여에 의해 acetylcholine 유발 혈관 이완은 증가되는 경향을 나타내었고, 전처치한 L-NAME, methylene blue에 의해 혈관 절편의 acetylcholine (ACh) 유발 이완은 억제되었으며 methylene blue에 의해 현저히 억제되었다. 그러나 세균 내독소를 투여하지 않은 군의 ACh 유발 혈관 이완 반응은 methylene blue에 의해서만 억제되었다. 결론적으로 세균 내독소에 의한 혈관 반응성 감소와 혈관 이완 반응은 NO가 발생되어 guanylyl cyclase를 활성화하여 유발된다고 생각되며, 세균 내독소에 의한 효과는 L-arginine NO pathway 보다는 cyclic GMP 신호전달계를 경유한 경로에서 더 많은 영향을 받는것으로 사료된다.

• 생명과학회지
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• 제25권9호
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• pp.984-992
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• 2015

혈근초(Sanguinaria canadensis)에서 처음 분리된 sanguinarine은 항산화, 항암 및 면역 증강 등의 효능이 있는 것으로 알려진 alkaloid 계열 물질 중의 하나이다. 본 연구에서는 인체간암 HepG2 세포를 대상으로 sanguinarine의 apoptosis 유도 효능 및 관련 기전 해석을 시도하였다. 본 연구의 결과에 의하면 sanguinarine은 HepG2 간암세포의 증식을 처리 농도 의존적으로 억제하였으며, 이는 apoptosis 유도와 연관성이 있었다. Sanguinarine에 의한 apoptosis 유도에는 Fas 및 Bax의 발현 증가, 미토콘드리아에서 세포질로의 cytochrome c 유리 및 MMPl (Δψm)의 소실을 동반하였다. Sanguinarine은 intrinsic 및 extrinsic apoptosis pathway의 활성에 관여하는 initiator caspase인 caspase-9와 -8의 활성과 effector caspase인 caspase-3의 활성 및 PARP 단백질의 단편화를 유발하였다. Sanguinarine은 또한 ROS의 생성을 촉진시켰으며, N-acetylcysteine 처리에 의한 ROS의 생성을 차단하였을 경우, sanguinarine에 의한 apoptosis 효능이 완벽하게 차단되었다. 아울러 sanguinarine은 Akt의 인산화를 억제한 반면, MAPKs의 인산화를 촉진시켰으며, 특히 PI3K와 ERK의 선택적 억제제는 sanguinarine에 의한 HepG2 간암세포의 증식을 더욱 억제시켰다. 따라서 sanguinarine에 의한 HepG2 간암세포의 apoptosis 유발에는 ROS 생성 의존적인 intrinsic 및 extrinsic signaling pathway가 동시에 활성화되며, PI3K/Akt 및 ERK 신호계가 관여함을 알 수 있었다.