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Kyu-shik Jeong,정원일,Jae-yong Chung,Mi-young An,Chae-yong Jung,Gyoung-jae Lee,Jong-soo Kang,Byeong-cheol Kang,Young-heun Jee,Bruce H Williams,Young-oh Kwon,Da-hee Jeong 대한수의학회 2003 Journal of Veterinary Science Vol.4 No.2
Cirrhosis Occurring in a Young Woodchuck (Marmota monax) Due to Vertical Transmission of Woodchuck Hepatitis Virus (WHV)Da-hee Jeong, Won-il Jeong, Jae-yong Chung, Mi-young An, Chae-yong Jung, Gyoung-jae Lee1, Jong-soo Kang1, Byeong-cheol Kang2, Young-heun Jee3, Bruce H Williams4, Young-oh Kwon5 and Kyu-shik Jeong*College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Korea1Shinwon Scientific Co., LTD, Research Institute, Suwon, Korea2Clinical Research Institute, Seoul National University, Seoul 110-744, Korea3College of Veterinary Medicine, Jeju National University, Jeju 690-756, Korea
Kang, Young-Jin,Kang, Sun-Young,Lee, Young-Soo,Park, Min-Kyu,Kim, Hye-Jung,Seo, Han-Geuk,Lee, Jae-Heun,YunChoi, Hye-Sook,Chang, Ki-Churl The Korean Society of Pharmacology 2004 The Korean Journal of Physiology & Pharmacology Vol.8 No.5
Nitric oxide (NO) has been suggested to act as a mediator of cytokine-induced effects of turn over of bone. Activation of the inducible nitric oxide synthase (iNOS) by inflammation has been related with apoptotic cell death in osteoblast. YS 49, a synthetic isoquinoline alkaloid, inhibits NO production in macrophages activated with cytokines. In the present study, we investigated the molecular mechanism of YS 49 to inhibit iNOS expression in ROS 17/2.8 cells, which were activated with combined treatment of inflammatory cytokines $(TNF-{\alpha},\;IFN-{\gamma})$ and lipopolysaccharide (LPS). Results indicated that YS 49 concentration-dependently reduced iNOS mRNA and protein expression, as evidenced by Northern and Western blot analysis, respectively. The underlying mechanism by which YS 49 suppressed iNOS expression was not to affect iNOS mRNA stability but to inhibit activation and translocation of $NF-_kB$ by preventing the degradation of its inhibitory protein $I_kB_{\alpha}$. As expected, YS 49 prevented NO-induced apoptotic cell death by sodium nitroprusside. Taken together, it is concluded that YS 49 inhibits iNOS expression by interfering with degradation of phosphorylated inhibitory $_kB_{\alpha}\;(p-I_kB_{\alpha})$. These actions may be beneficial for the treatment of inflammation of the joint, such as rheumatoid arthritis.
Kang, Soo-Kyung,Cha, Seung-Heun,Jeon, Hyo-Gon Mary Ann Liebert 2006 STEM CELLS AND DEVELOPMENT Vol.15 No.2
<P>Acetylation of histones and nonhistone proteins is an important post-translational modification involved in the regulation of gene expression in mammalian cells. Dysfunction of histone acetyltransferase (HAT) is often associated with the manifestation of several diseases. In this report, HATs are new targets for the development of therapeutics. Our studies first proved that curcumin induces histone hypoacetylation in brain cancer cells and finally induces apoptotic cell death through a (PARP)- and caspase 3-mediated manner. In addition, curcumin induces recontrolling of neural stem cell fates. It induces effective neurogenesis, synaptogenesis, and migration of neural progenitor cells in vitro in brain-derived adult neural stem cells. We also confirmed the neurogenic effect of curcumin in our in vivo experiments. Curcumin actively suppressed differentiation in astrocytes while promoting differentiation into the neurons associated with decrease of histone H3 and H4 acetylation. We suggest that histone hypoacetylation plays an important role in determine stem cell fate through controlling the simultaneous expression of many genes. Thus, the present finding that curcumin, a nontoxic dietary compound, is a histone acetyltransferase inhibitor would supply a new window to understand further the molecular mechanism of histone acetylase inhibitors (HAI) in cancer and neural stem cells and provide a new target molecule for treating central nervous system disorders.</P>
백서 해마에서 카이닌산 유도 경련에 의한 JNK 경유 신호전달경로 활성화의 발달 단계에 따른 변화
김종흔,정희연,노명선,안용민,강웅구,김용식,조수철 大韓神經精神醫學會 2001 신경정신의학 Vol.40 No.5
연구목적 : 어린 백서의 해마에서 전기경련충격(electroconvulsive shock, ECS) 후 활성화되는 것으로 알려져 있는 MAPK계 신호전달경로가 카이닌산(Kainic acid, KA)에 의한 경련 후 어떤 양상으로 활성화되는 지를 초기 발달 단계에 따라서 관찰하고자 하였다. 방 법 : 생후 7일, 14일, 21일 된 어린 백서와 성년 백서의 해마에서 면역블롯 방법으로 MAPK계 효소의 인산화 효소 중 하나인 SAPK/ERK kinase-1(SEK-1), MAPK계 효소인 c-Jun N terminal protein kinase(JNK), 전사인자 c-Jun 및 조기유전자 단백질 Fos의 단백질 양과 기저 인산화를 측정하였고, 백서에게 KA를 주사하여 경련을 유발한 후 위 단백질들의 인산화 변화의 양상을 같은 방법으로 관찰하였다. 결 과 : SEK-1, JNK, c-Jun 모두 연령 증가에 따른 단백질 양 자체에는 변화가 없었다. JNK와 c-Jun은 기저 인산화의 양적 변화도 없었으나 SEK-1의 경우 기저 인산화 양이 생후 7일에 가장 높고 이후 연령이 높아짐에 따라 감소하였다. JNK의 경우 KA 주사 후 인산화 변화 양상이 관찰되지 않았으나 SEK-1과 c-Jun은 생후 14일부터 연령의 증가와 함께 인산화 양도 증가하였다. Fos 역시 생후 7일부터 발현되어 연령의 증가와 함께 발현양이 증가하였다. 결 론 : 백서 해마에서의 MAPK계 신호전달계의 성숙은 연령의 증가에 따라, 또 신호전달 물질에 따라 차이를 보였다. KA 유도 경련 후 JNK는 생후 21일까지도 활성화가 되지 않는 것으로 보아, 세포주에서 알려진 SEK-1 - JNK-c-Jun - Fos로 연결되는 신호전달 경로가 어린 백서의 해마에서는 적용될 수 없음을 시사한다. Objective : We observed the developmental pattern of activation of MAPK signal transduction pathways known to be activated by eletroconvulsive shock(ECS) in young rat hippocampus after kainic acid(KA)-induced seizure. Methods : We used the method of immunoblotting for examining the basal protein amount and basal level of phosphorylation of MAPK kinase(SAPK/ERK kinase -1, SEK-1), MAPK(c-Jun N terminal protein kinase, JNK), transcription factor(c-Jun) and immediate early gene proteins(Fos) in rat hippocampus at postnatal day 7, 14 and 21, respectively. We also examined the changes of phosphorylation of those proteins after kainic acid-induced seizure in the same way. Results : The basal protein amounts of SEK-1, JNK, and c-Jun did not show age-dependent changes and basal level of phosphorylation of JNK and c-Jun remains unchanged throughout the early developmental period. The basal level of phosphorylation of SEK-1 was peaked at postnatal 7 days and then decreased with aging. After kainic acid-induced seizure, the change of phosphorylation of JNK was not observed but those of SEK-1 and c-Jun increased after postnatal day 14. The expression of Fos was observed at postnatal day 7 and also increased with aging. Conclusion : These results show that the MAPK signal transduction system in rat hippocampus matures in accordance with aging, but the process of maturation differs depending specific proteins. This study suggests the signal transduction cascade(SEK-1 - JNK - c-Jun - Fos) which is well established in cell line studies may not be applied to rat hipposcampus because we could not observe the activation of JNK after KA-induced seizure in young rat hippocampus.
Young Jin Kang,Sun Young Kang,Young Soo Lee,Min Kyu Park,Hye Jung Kim,Han Geuk Seo,Jae Heun Lee,Hye Sook Yun-Choi,Ki Churl Chang 대한생리학회-대한약리학회 2004 The Korean Journal of Physiology & Pharmacology Vol.8 No.5
Nitric oxide (NO) has been suggested to act as a mediator of cytokine-induced effects of turn over of bone. Activation of the inducible nitric oxide synthase (iNOS) by inflammation has been related with apoptotic cell death in osteoblast. YS 49, a synthetic isoquinoline alkaloid, inhibits NO production in macrophages activated with cytokines. In the present study, we investigated the molecular mechanism of YS 49 to inhibit iNOS expression in ROS 17/2.8 cells, which were activated with combined treatment of inflammatory cytokines (TNF-α, IFN-γ) and lipopolysaccharide (LPS). Results indicated that YS 49 concentration-dependently reduced iNOS mRNA and protein expression, as evidenced by Northern and Western blot analysis, respectively. The underlying mechanism by which YS 49 suppressed iNOS expression was not to affect iNOS mRNA stability but to inhibit activation and translocation of NF-κB by preventing the degradation of its inhibitory protein IκBα. As expected, YS 49 prevented NO-induced apoptotic cell death by sodium nitroprusside. Taken together, it is concluded that YS 49 inhibits iNOS expression by interfering with degradation of phosphorylated inhibitory κBα (p-IκBα). These actions may be beneficial for the treatment of inflammation of the joint, such as rheumatoid arthritis.
Chong, Won-Seog,Kang, Sun-Young,Kang, Young-Jin,Park, Min-Kyu,Lee, Young-Soo,Kim, Hye-Jung,Seo, Han-Geuk,Lee, Jae-Heun,ChoiYun, Hye-Sook,Chang, Ki-Churl The Korean Society of Pharmacology 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.5
Endothelium, particularly pulmonary endothelium, is predisposed to injury by reactive oxygen species (ROS) and their derivatives. Heme oxygenase (HO) has been demonstrated to provide cytoprotective effects in models of oxidant-induced cellular and tissue injuries. In the present study, we investigated the effects of YS 49 against oxidant [tert-butylhydroperoxide (TBH)]-induced injury using cultured sheep pulmonary artery endothelial cells (SPAECs). The viability of SPAECs was determined by quantifying reduction of a fluorogenic indicator Alamar blue. We found that TBH decreased cell viability in a timeand concentration-dependent manner. YS 49 concentration- and time-dependently increased HO-1 induction on SPAECs. As expected, YS 49 significantly decreased the TBH-induced cellular injury. In the presence of zinc protophorphyrin, HO-1 inhibitor, effect of YS 49 was significantly inhibited, indicating that HO-1 plays a protective role for YS 49. Furthermore, YS 49 showed free radical scavenging activity as evidenced by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and inhibition of lipid peroxidation. However, YS 49 did not inhibit apoptosis induced by lipopolysaccharide (LPS) in SPAECs. Taken together, HO-1 induction along with strong antioxidant action of YS 49 may be responsible for inhibition of TBH-induced injury in SPAECs.
Oh Hwa Min,Kang Young Jin,Kim Sun Hee,Lee Young Soo,Park Min Kyu,Heo Ja Myung,Sun Jin Ji,Kim Hyo Jung,Kang Eun Sil,Kim Hye Jung,Sea Han Geuk,Lee Jae Heun,YunChoi Hye Sook The Pharmaceutical Society of Korea 2005 Archives of Pharmacal Research Vol.28 No.3
It has been suggested that nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) may act as a mediator of cytokine-induced effects on bone turn-over. NO is also recognized as an important factor in bone remodeling, i.e., participating in osteoblast apoptosis in an arthritic joint. The components of Agastache rugosa are known to have many pharmacological activities. In the present study, we investigated the effects of Agastache rugosa leaf extract (ELAR) on NO production and the iNOS expression in ROS 17/2.8 cells activated by a mixture of inflammatory cytokines including TNF-$alpha$ and IL-1$\beta$. A preincubation with ELAR significantly and concentration-dependently reduced the expression of iNOS protein in ROS 17/2.8 cells activated with the cytokine mixture. Consequently, the NO production was also significantly reduced by ELAR with an IC$_{50}$ of 0.75 mg/mL. The inhibitory mechanism of iNOS induction by ELAR prevented the activation and translocation of NF-$\kappa$B (p65) to the nucleus from the cytosol fraction. Furthermore, ELAR concentration-dependently reduced the cellular toxicity induced by sodium nitroprusside, an NO-donor. These results suggest that ELAR may be beneficial in NO-mediated inflammatory conditions such as osteoporosis.