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Paraquat 투여 백서에서 Cyclophosphamide와 Dexamethasone의 치료 효과
신정철,신양수,유병전,임현성,정태흥,박찬국,오금탁,이병래 朝鮮大學校 附設 醫學硏究所 1991 The Medical Journal of Chosun University Vol.16 No.1
Paraquat (N,N'-dimethy 1-4,4'bipyrydinium : Gramoxone^(R), a widely used herbicide, is extremely toxic to all green plants and many eukaryotic organisms. In human, paraquat intoxication leads to multiple organ failure, it preferentially damages the lung, kidney and liver and may result in death. The participation of superoxide in initiating tissue damage by administration of paraquat is well known in which one electron reduction of paraquat leads to the formation of radical species which react with molecular oxygen to give superoxide. This process initiates immunological changes with the activation of neutrophilic leukocytes, which is related to further production of superoxide. In this experiment, therapeutic effects of cyclophosphamide and dexamethasone on blood cell count, malondialdehyde as a indicator of lipid peroxidation, and antioxidant enzymes levels in the lung, liver and kidney of paraquat intoxicated rats were inbestigated. The WBC count were significantly decreased by combined treatment of cyclophosphamide and dexamethasone in paraquat intoxicated rats at 3 and 5 days but RBC count were not changed. The contents of malondialdehyde were significantly decreased in the lung and Kidney by combined treatment at 10 days after paraquat intoxication. The catalase acitvities were markedly increased in the lung and liver of rats at 10 days after paraquat intoxication, and superoxide dismutase activities showed minimal changes in the lung, liver and kidney of rats by combined treatment. These results suggest that paraquat induced tissue damage in rats can be redeced by combined administration of cyclophosphamide and dexamethasone.
Jeon, Byeong Tak,Jeong, Eun Ae,Shin, Hyun Joo,Lee, Younghyurk,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob American Diabetes Association 2012 Diabetes Vol.61 No.6
<P><B/></P><P>Obesity-induced diabetes is associated with chronic inflammation and is considered a risk factor for neurodegeneration. We tested the hypothesis that an AMP-activated protein kinase activator, resveratrol (RES), which is known to exert potent anti-inflammatory effects, would attenuate peripheral and central inflammation and improve memory deficit in mice fed a high-fat diet (HFD). C57BL/6J mice were fed an HFD or an HFD supplemented with RES for 20 weeks. Metabolic parameters in serum were evaluated, and Western blot analysis and immunohistochemistry in peripheral organs and brain were completed. We used the Morris water maze test to study the role of RES on memory function in HFD-treated mice. RES treatment reduced hepatic steatosis, macrophage infiltration, and insulin resistance in HFD-fed mice. In the hippocampus of HFD-fed mice, the protein levels of tumor necrosis factor-α and Iba-1 expression were reduced by RES treatment. Choline acetyltransferase was increased, and the phosphorylation of tau was decreased in the hippocampus of HFD-fed mice upon RES treatment. In particular, we found that RES significantly improved memory deficit in HFD-fed mice. These findings indicate that RES reverses obesity-related peripheral and central inflammation and metabolic derangements and improves memory deficit in HFD-fed diabetic mice.</P>
Jeon, Byeong Tak,Jeong, Eun Ae,Park, Sun-Young,Son, Hyeonwi,Shin, Hyun Joo,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Harwood Academic Publishers 2013 Neurotoxicity research Vol.23 No.3
<P>Rho-associated coil kinase (ROCK) inhibitors reportedly prevent neurodegeneration, and abnormal ROCK activation in the central nervous system induces neurite collapse and retraction. However, it is unclear whether the ROCK inhibitor Y-27632 directly protects hippocampal neurons from excitotoxicity. Here, we determined the effects of Y-27632 on neuroprotection following kainic acid (KA)-induced seizures in mice and during glutamate-induced excitotoxicity in HT22 cells. One day after Y-27632 injection, mice were treated with KA and killed 1-2 days later. Fluoro-Jade B and rapid Golgi staining showed that Y-27632 protected against KA-induced neurodegeneration and neurite dystrophy. Y-27632 inhibited increases in hippocampal RhoA and ROCK2 in KA-treated mice as determined by western blot analysis. Immunohistochemical analysis revealed ROCK2-positive neurons and astrocytes in the KA-treated hippocampus. In HT22 cells, Y-27632 also protected neurons and neurite formation during glutamate-induced excitotoxicity in vitro. These results indicate that ROCK inhibition modulates neurite growth and protects neurons from excitotoxicity-induced cell death.</P>
H<sub>2</sub>O<sub>2</sub>-induced up-regulation of CatSper3 in mouse brain
Kim, Chang-Woon,Tak, Hyun-Min,Kim, Gyu-Tae,Mun, Yun-Ja,Jeon, Byeong Tak,Kim, Hyun Joon,Roh, Gu Seob,Han, Jaehee,Kang, Dawon Wiley Subscription Services, Inc., A Wiley Company 2010 Molecular reproduction and development Vol.77 No.8
Yi, Chin-Ok,Jeon, Byeong Tak,Shin, Hyun Joo,Jeong, Eun Ae,Chang, Ki Churl,Lee, Jung Eun,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Korean Association of Anatomists 2011 Anatomy & Cell Biology Vol.44 No.3
<P>AMP-activated protein kinase (AMPK), an enzyme involved in energy homeostasis, regulates inflammatory responses, but its precise mechanisms are not fully understood. Recent evidence has shown that resveratrol (RES), an AMPK activator, reduces prostaglandin E<SUB>2</SUB> production in lipopolysaccharide (LPS)-treated microglia. Here, we examined the effect of RES on nuclear factor kappa B (NF-κB) dependent cyclooxygenase (COX)-2 activation in LPS-treated RWA 264.7 macrophages. We found that treatment with RES increased AMPK activation. AMPK and acetyl CoA carboxylase phosphorylation were attenuated in cells treated with LPS+RES, compared to cells treated with LPS alone. RES inhibited tumor necrosis factor (TNF)-α and TNF receptor 1 in LPS-treated cells. Finally, RES inhibited LPS-induced NF-κB translocation into the nucleus and COX-2 expression. Moreover, the effects of 5-aminoimidazole-4-carboxamide ribose and compound C were consistent with the effects of RES in LPS-treated cells. Taken together, these results suggest that the anti-inflammatory action of RES in RAW 264.7 macrophages is dependent on AMPK activation and is associated with inhibition of the LPS-stimulated NF-κB-dependent COX-2 signaling pathway.</P>
Jang, In-Seok,Jeon, Byeong-Tak,Jeong, Eun-Ae,Kim, Eun-Jin,Kang, Da-Won,Lee, Jong-Sil,Jeong, Baek-Geun,Kim, Jin-Hyun,Choi, Bong-Hoi,Lee, Jung-Eun,Kim, Jong-Woo,Choi, Jun-Young,Roh, Gu-Seob The Korean Society of Pharmacology 2012 The Korean Journal of Physiology & Pharmacology Vol.16 No.3
Squamous cell carcinoma (SCC) and adenocarcinoma (AC) are the major histological types of non-small cell lung carcinoma (NSCLC). Although both SCCs and ACs have been characterized histologically and clinically, the precise mechanisms underlying their migration and invasion are not yet known. Here, we address the involvement in NSCLC of the p21-associated kinase1 (Pak1)/LIM kinase1 (LIMK1)/cofilin pathway, which recently has been reported to play a critical role in tumor migration and invasion. The Pak1/LIMK1/cofilin pathway was evaluated in tumors from SCC (n=35) and AC (n=35) patients and in SCC- and AC-type cell lines by western blotting, immunohistochemistry, and in vitro migration and invasion assays. The levels of phosphorylated Pak1, LIMK1, and cofilin in lung tumor tissues from SCC patients were increased as compared to normal tissues. In addition, immunohistochemistry showed greater expression of phosphorylated cofilin in SCC tissues. Expression of phosphorylated Pak1 and LIMK1 proteins was also significantly higher in SCC-type cells than in AC-type cells. Moreover, migration and invasion assays revealed that a higher percentage of SCC type cells exhibited migration and invasion compared to AC type cells. Migration was also decreased in LIMK1 knockdown SK-MES-1 cells. These findings suggest that the activation of the Pak1/LIMK1/cofilin pathway could preferentially contribute to greater tumor migration and invasion in SCC, relative to that in AC.
Jeong, Eun Ae,Jeon, Byeong Tak,Shin, Hyun Joo,Kim, Nayoung,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Elsevier 2011 Experimental neurology Vol.232 No.2
<P><B>Abstract</B></P><P>Similar to fasting, the ketogenic diet (KD) has anti-inflammatory effects and protects against excitotoxicity-mediated neuronal cell death. Recent studies have shown that peroxisome proliferator-activated receptor (PPAR)γ has anti-inflammatory effects in seizure animal models. However, the exact mechanisms underlying the anti-inflammatory effects of the KD have not been determined for seizures. Here we investigated the effect of the KD and acetoacetate (AA) on neuroinflammation in a seizure animal model and glutamate-treated HT22 cells, respectively. Mice were fed the KD for 4weeks and sacrificed 2 or 6h after KA injection. The KD reduced hippocampal tumor necrosis factor alpha (TNF-α) levels and nuclear factor (NF)-κB translocation into the nucleus 2h after KA treatment. KD-induced PPARγ activation was decreased by KA in neurons as assessed by western blotting and immunofluorescence. Finally, the KD inhibited cyclooxygenase (COX)-2 and microsomal prostaglandin E<SUB>2</SUB> synthase-1 (mPGES-1) expression in the hippocampus 6h after KA treatment. AA treatment also protected against glutamate-induced cell death in HT22 cells by reducing TNF-α and PPARγ-mediated COX-2 expression. Thus, the KD may inhibit neuroinflammation by suppressing a COX-2-dependent pathway via activation of PPARγ by the KD or AA.</P> <P><B>Highlights</B></P><P>► Ketogenic diet (KD) attenuated neuroinflammation in the kainic acid (KA)-induced seizure mice. ► KD induces activation of PPARγ expression in the mouse hippocampus. ► KD inhibits NF-κB-mediated COX-2 expression in the KA-treated hippocampus.</P>
Shin, Hyun Joo,Jeon, Byeong Tak,Kim, Jungmee,Jeong, Eun Ae,Kim, Myeung Ju,Lee, Dong Hoon,Kim, Hyun Joon,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung,Roh, Gu Seob Springer 2012 Journal of neural transmission Vol.119 No.6
<P>Calcineurin (CaN)-mediated excitotoxicity impairs 관-aminobutyric acid (GABA) transmission and induces neuronal apoptosis. Ca(2+)-dependent K(+)-Cl(-) cotransporter 2 (KCC2) participates in GABAergic inhibitory transmission. However, the mechanism by which CaN mediates GABA receptor-mediated KCC2 in seizures is not fully understood. In the present study, we investigated the altered expression of KCC2 and the effects of the CaN inhibitor FK506 on KCC2 expression in the mouse hippocampus following kainic acid (KA) treatment. FK506 was injected twice 24 h and 30 min before KA treatment and then mice were treated with KA and killed 2 days later. FK506 had anticonvulsant effect on KA-induced seizure activities. CaN cleavage was evident in the hippocampus 24 h after KA treatment. FK506 pretreatment blocked the truncation of CaN in the KA-treated hippocampus. Cresyl violet and TUNEL staining showed that FK506 prevented KA-induced hippocampal cell death. In particular, Western blot analysis showed that KCC2 expression was time dependent, with a peak at 6 h and a return to decreased levels at 48 h, whereas FK506 pretreatment inhibited the KA-induced decrease in KCC2 expression in the hippocampus. Immunofluorescence showed that FK506 pretreatment protected the loss of inhibitory GABAergic KCC2-expressing neurons following KA treatment. Taken together, these results provide evidence that altered KCC2 expression may be associated with Ca(2+)-mediated seizure activity and indicate that neuron-specific KCC2 may be involved in neuroprotection after seizures.</P>
Chin-Ok Yi,Byeong Tak Jeon,Hyun Joo Shin,Eun Ae Jeong,Ki Churl Chang,Jung Eun Lee,Dong Hoon Lee,Hyun Joon Kim,Sang Soo Kang,Gyeong Jae Cho,Wan Sung Choi,Gu Seob Roh 대한해부학회 2011 Anatomy & Cell Biology Vol.44 No.3
AMP-activated protein kinase (AMPK), an enzyme involved in energy homeostasis, regulates inflammatory responses, but its precise mechanisms are not fully understood. Recent evidence has shown that resveratrol (RES), an AMPK activator, reduces prostaglandin E2 production in lipopolysaccharide (LPS)-treated microglia. Here, we examined the effect of RES on nuclear factor kappa B (NF-κB) dependent cyclooxygenase (COX)-2 activation in LPS-treated RWA 264.7 macrophages. We found that treatment with RES increased AMPK activation. AMPK and acetyl CoA carboxylase phosphorylation were attenuated in cells treated with LPS+RES, compared to cells treated with LPS alone. RES inhibited tumor necrosis factor (TNF)-α and TNF receptor 1 in LPS-treated cells. Finally, RES inhibited LPS-induced NF-κB translocation into the nucleus and COX-2 expression. Moreover, the effects of 5-aminoimidazole-4-carboxamide ribose and compound C were consistent with the effects of RES in LPS-treated cells. Taken together, these results suggest that the anti-inflammatory action of RES in RAW 264.7 macrophages is dependent on AMPK activation and is associated with inhibition of the LPS-stimulated NF-κB-dependent COX-2 signaling pathway.
Eun Ae Jeong,Byeong Tak Jeon,Jeong Bin Kim,Joon Soo Kim,Yong Woon Cho,Dong Hoon Lee,Hyun Joon Kim,Sang Soo Kang,Gyeong Jae Cho,Wan Sung Choi,Gu Seob Roh 대한해부학회 2010 Anatomy & Cell Biology Vol.43 No.2
Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3ζ and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3ζ-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3ζ at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.