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Kong, Pil-Jae,Park, Jong-Ik,Kwon, Oh-Yoon,Han, Yoon-Hee,Kim, Soo-Young,Lee, Su-Nam,Son, Hee-Jeong,Kim, Sung-Soo The Korean Society of Pharmacology 2007 The Korean Journal of Physiology & Pharmacology Vol.11 No.1
Antioxidant properties have been proposed as a mechanism for the putative anti-inflammatory effects of phenolic compounds. To reveal the relationship between antioxidant activity and anti-inflammatory effects of various antioxidants, we measured 1, 1-diphenyl-2-picryhydrazyl(DPPH)-reducing activity and examined the inhibitory effects on LPS-induced inflammation-related gene expression in the BV2 microglial cell line. Lipopolysaccharide(LPS)(0.2 ${\mu}g/ml$) was used with or without antioxidants to treat cells, and the regulation of iNOS and cytokine gene expression was monitored using an RNase protection assay(RPA). Although, all tested antioxidants had similar DPPH-reducing activity and inhibited nitrite production, but the curcuminoid antioxidants(ferulic acid, caffeic acid, and curcumin) inhibited LPS-induced gene expression(iNOS, $TNF-\alpha,\;IL-1{\beta}$, IL-6, and IL-1 Ra) in a concentration-dependent manner. Other tested antioxidants did not exhibit the same effects; N-acetylcysteine(NAC) only began to suppress $IL-1{\beta}$ gene expression just below the concentration at which cytotoxicity occurred. Moreover, the antioxidant potency of curcuminoids appeared to have no correlation with anti-inflammatory potency. Only curcumin could inhibit LPS-induced microglial activation at a micromolar level. These data suggest that curcumin may be a safe antioxidant possessing anti-inflammatory activity.
Kong, Pil-Jae,Kim, Yu-Mi,Lee, Hee-Jae,Kim, Sung-Soo,Yoo, Eun-Sook,Chun, Wan-Joo The Korean Society of Pharmacology 2007 The Korean Journal of Physiology & Pharmacology Vol.11 No.5
Neuronal death is a common characteristic hallmark of a variety of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease. However, there have been no effective drugs to successfully prevent neuronal death in those diseases, whereas oriental medicinal plants have to possess valuable therapeutic potentials to treat neurodegenerative diseases. In the present study, in an attempt to provide neuroprotective agents from natural plants, 80% methanol extracts of a wide range of medicinal plants, which are native to Jeju Island in Korea, were prepared and their protective effects on hydrogen peroxide-induced apoptotic cell death were examined. Among those tested, extracts from Smilax china and Saururus chinesis significantly decreased hydrogen peroxide-induced apoptotic cell death. The extracts attenuated hydrogen peroxide($H_2O_2$)-induced caspase-3 activation in a dose-dependent manner. Further, plant extracts restored $H_2O_2$-induced depletion of intracellular glutathione, a major endogenous antioxidant. The data suggest that Jeju native medicinal plants could potentially be used as therapeutic agents for treating or preventing neurodegenerative diseases in which oxidative stress is implicated.
Kong, Pil-Jae,Byun, Jong-Seon,Lim, So-Young,Lee, Jae-Jun,Hong, Sung-Jun,Kwon, Kwang-Jun,Kim, Sung-Soo The Korean Society of Pharmacology 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.2
Melatonin has been reported to protect neurons from a variety of neurotoxicity. However, the underlying mechanism by which melatonin exerts its neuroprotective property has not yet been clearly understood. We previously demonstrated that melatonin protected kainic acid-induced neuronal cell death in mouse hippocampus, accompanied by sustained activation of Akt, a critical mediator of neuronal survival. To further elucidate the neuroprotective action of melatonin, we examined in the present study the causal mechanism how Akt signaling pathway is regulated by melatonin in a rat primary astrocyte culture model. Melatonin resulted in increased astrocytic Akt phosphorylation, which was significantly decreased with wortmannin, a specific inhibitor of PI3K, suggesting that activation of Akt by melatonin is mediated through the PI3K-Akt signaling pathway. Furthermore, increased Akt activation was also significantly decreased with luzindole, a non-selective melatonin receptor antagonist. As downstream signaling pathway of Akt activation, increased levels of CREB phoshorylation and GDNF expression were observed, which were also attenuated with wortmannin and luzindole. These results strongly suggest that melatonin exerts its neuroprotective property in astrocytes through the activation of plasma membrane receptors and then PI3K-Akt signaling pathway.
Pil-Jae Kong,Jong-Ik Park,Oh-Yoon Kwon,Yoon Hee Han,Soo Young Kim,Su Nam Lee,Hee Jeong Son,Sung-Soo Kim 대한생리학회-대한약리학회 2007 The Korean Journal of Physiology & Pharmacology Vol.11 No.1
Antioxidant properties have been proposed as a mechanism for the putative anti-inflammatory effects of phenolic compounds. To reveal the relationship between antioxidant activity and anti-inflammatory effects of various antioxidants, we measured 1, 1-diphenyl-2-picryhydrazyl (DPPH)-reducing activity and examined the inhibitory effects on LPS-induced inflammation-related gene expression in the BV2 microglial cell line. Lipopolysaccharide (LPS) (0.2μg/ml) was used with or without antioxidants to treat cells, and the regulation of iNOS and cytokine gene expression was monitored using an RNase protection assay (RPA). Although, all tested antioxidants had similar DPPH-reducing activity and inhibited nitrite production, but the curcuminoid antioxidants (ferulic acid, caffeic acid, and curcumin) inhibited LPS-induced gene expression (iNOS, TNF-α, IL-1β, IL-6, and IL-1 Ra) in a concentration-dependent manner. Other tested antioxidants did not exhibit the same effects; N-acetylcysteine (NAC) only began to suppress IL-1β gene expression just below the concentration at which cytotoxicity occurred. Moreover, the antioxidant potency of curcuminoids appeared to have no correlation with anti- inflammatory potency. Only curcumin could inhibit LPS-induced microglial activation at a micromolar level. These data suggest that curcumin may be a safe antioxidant possessing anti-inflammatory activity.
Pil-Jae Kong,Yu-Mi Kim,Hee Jae Lee,Sung-Soo Kim,Eun Sook Yoo,Wanjoo Chun 대한생리학회-대한약리학회 2007 The Korean Journal of Physiology & Pharmacology Vol.21 No.1
Neuronal death is a common characteristic hallmark of a variety of neurodegenerative disorders including Alzheimer s disease and Parkinson s disease. However, there have been no effective drugs to successfully prevent neuronal death in those diseases, whereas oriental medicinal plants have to possess valuable therapeutic potentials to treat neurodegenerative diseases. In the present study, in an attempt to provide neuroprotective agents from natural plants, 80% methanol extracts of a wide range of medicinal plants, which are native to Jeju Island in Korea, were prepared and their protective effects on hydrogen peroxide-induced apoptotic cell death were examined. Among those tested, extracts from Smilax china and Saururus chinesis significantly decreased hydrogen peroxide-induced apoptotic cell death. The extracts attenuated hydrogen peroxide (H2O2)-induced caspase-3 activation in a dose-dependent manner. Further, plant extracts restored H2O2-induced depletion of intracellular glutathione, a major endogenous antioxidant. The data suggest that Jeju native medicinal plants could potentially be used as therapeutic agents for treating or preventing neurodegenerative diseases in which oxidative stress is implicated.
Pil-Jae Kong,Jong-Seon Byun,So-Young Lim,Jae-Jun Lee,Sung-Jun Hong,Kwang-Jun Kwon,Sung-Soo Kim 대한생리학회-대한약리학회 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.2
Melatonin has been reported to protect neurons from a variety of neurotoxicity. However, the underlying mechanism by which melatonin exerts its neuroprotective property has not yet been clearly understood. We previously demonstrated that melatonin protected kainic acid-induced neuronal cell death in mouse hippocampus, accompanied by sustained activation of Akt, a critical mediator of neuronal survival. To further elucidate the neuroprotective action of melatonin, we examined in the present study the causal mechanism how Akt signaling pathway is regulated by melatonin in a rat primary astrocyte culture model. Melatonin resulted in increased astrocytic Akt phosphorylation, which was significantly decreased with wortmannin, a specific inhibitor of PI3K, suggesting that activation of Akt by melatonin is mediated through the PI3K-Akt signaling pathway. Furthermore, increased Akt activation was also significantly decreased with luzindole, a non-selective melatonin receptor antagonist. As downstream signaling pathway of Akt activation, increased levels of CREB phoshorylation and GDNF expression were observed, which were also attenuated with wortmannin and luzindole. These results strongly suggest that melatonin exerts its neuroprotective property in astrocytes through the activation of plasma membrane receptors and then PI3K-Akt signaling pathway.
CCD Signal Processing for Optimal Non-Uniformity Correction
Kong, Jong-Pil,Lee, Song-Jae The Korean Society of Remote Sensing 2010 大韓遠隔探査學會誌 Vol.26 No.6
The performance of the payload Electro-Optical System (EOS) in satellite system is affected by various factors, such as optics design, camera electronics design, and the characteristics of the CCD (Charge Coupled Device) used, etc. Of these factors, the camera electronics design is somewhat unique in that its operational parameters can be adjusted even after the satellite launch. In this paper, the effect of video gain on the non-uniformity correction performance is addressed. And a new optimal non-uniformity correction scheme is proposed and analyzed using the data from real camera electronics unit based on a TDI (Time Delayed Integration) type of CCD. The test results show that the performance of the conventional non-uniformity correction scheme is affected significantly when the video gain is added. On the other hand, in our proposed scheme, the performance is not dependent on the video gain. The insensitivity of the non-uniformity performance on the video-gain is mainly due to the fact that the correction is performed after the dark signal is subtracted from system response.