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Park, Channy,So, Hong Seob,Kim, Se Jin,Youn, Myung Ja,Moon, Byung-Soon,Shin, Sun-Ho,Lee, In,Moon, Seong-Keun,Park, Raekil Institute for Advanced Research in Asian Science a 2006 The American journal of Chinese medicine Vol.34 No.4
<P>Samul extract, containing Radix Rehmanniae, Radix Angelicae Gigantis, Radix Paeoniae, and Rhizoma Cnidii, has been traditionally used for treatment of ischemic heart and brain damages in Oriental medicine. However, little is known about the mechanism by which Samul rescues cells from cytotoxic damage. This study was designed to investigate the protective mechanisms of Samul on H(2)O(2)-induced death of H9c2 cells. Treatment with H(2)O(2) markedly decreased the viability of H9c2 cells in a dose- and time-dependent manner, which was significantly prevented by pre-treatment with Samul. The nature of death of H9c2 cells by H(2)O(2) was demonstrated by apoptotic features, including ladder-pattern fragmentation of genomic DNA and chromatin condensation, which were markedly abolished by pretreatment of Samul in H(2)O(2)-treated cells. We further demonstrated that MEK inhibitor, PD98059, dose-dependently attenuated the protective effects of Samul against H(2)O(2), whereas inhibitors of Jnk and p38 did not. Consistently, Samul induced the early phosphorylation of Erk, p44, in H(2)O(2)-treated cells. In addition, treatment with Samul also resulted in an increase of expression of anti-apotogenic Bcl2 protein, which was decreased by H(2)O(2). However, it inhibited the expression of apotogenic Bax protein in H(2)O(2)-treated cells. Taken together, these results suggest that the protective effects of Samul against oxidative damage may be achieved via activation of MAP kinase, Erk as well as Bcl2 family proteins.</P>
Park, Channy,Ji, Hye-Min,Kim, Se-Jin,Kil, Sung-Hee,Lee, Joon No,Kwak, Seongae,Choe, Seong-Kyu,Park, Raekil UNKNOWN 2017 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.39 No.4
<P>Fenofibrate, an activator of peroxisome proliferator-activated receptors (PPARs), has been shown to protect the kidneys and brain cells from oxidative stress; however, its role in preventing hearing loss has not been reported to date, at least to the best of our knowledge. In this study, we demonstrated the protective effects of fenofibrate against gentamicin (GM)-induced ototoxicity. We found that the auditory brainstem response threshold which was increased by GM was significantly reduced by pre-treatment with fenofibrate in rats. In cochlear explants, the disruption of hair cell layers by GM was also markedly attenuated by pre-treatment with fenofibrate. In addition, fenofibrate almost completely abolished GM-induced reactive oxygen species generation, which seemed to be mediated at least in part by the restoration of the expression of PPAR-α-dependent antioxidant enzymes, including catalase and superoxide dismutase (SOD)-1. Of note, fenofibrate markedly increased the expression of heme oxygenase-1 (HO-1) which was also induced to a certain degree by GM alone. The induced expression of HO-1 by fenofibrate appeared to be essential for mediating the protective effects of fenofibrate, as the inhibition of HO-1 activity significantly diminished the protective effects of fenofibrate against the GM-mediated death of sensory hair cells in cochlea explant culture, as well as in zebrafish neuromasts. These results suggest that fenofibrate protects sensory hair cells from GM-induced toxicity by upregulating PPAR-α-dependent antioxidant enzymes, including HO-1. Our results provide insight into the preventive therapy for hearing loss caused by aminoglycoside antibiotics.</P>
TRAIL-Mediated Apoptosis in Human Liver Chang Cells
Channy Park,Sung-Wook Hong,Sung-Ho Jin,Nam-song Kim,Kyung-Ho Cho,Jin-Ho Cheon,Jae-Yeon Ahn,Jung-ku Yang,Raekil Park 대한암학회 2003 Cancer Research and Treatment Vol.35 No.4
Purpose: Tumor necrosis factor (TNF)-related apoptosisinducing ligand (TRAIL)/APO-2L is a member of theTNF family that can kill a wide variety of tumor cells, butnot normal cells. This study was designed to investigatethe down stream target proteins in TRAIL-mediated apoptosisof human liver, Chang cells.Materials and Methods: The expressions of DR4/DR5in hepatoma cells, including Chang, HepG2 and Hep3Bcells, were determined by RT-PCR. Cell viability was measuredby MTT assay and apoptosis was assessed by DNAfragmentation assay. The catalytic activity of caspasefamilyproteases, including caspase-3 and -9, was testedby using fluorogenic biosubstrates. Expression of apoptoticmediators, including procaspase-3 and PARP proteins,was measured by Western blotting. The expressionprofile of proteins in Chang cells by using two-dimensional(2-D) gel electrophoresis and MALDI-TOF.Results: The results demonstrated that TRAIL (100 ng/ml) induced the apoptotic death of Chang cells, as characterizedby the ladder-pattern fragmentation of genomicDNA. TRAIL increased the enzymatic activity of caspase-3, corresponding to the time of appearance of cleavedPARP and caspase-9. In 2-D gel electrophoresis and MALDITOFanalysis, the comparison of control versus apoptoticcells in the protein expressions revealed that signalintensity of 7 spots were decreased, whereas 6 spots wereincreased among 300 spots. These spots were resolved andidentified as a protein information by MALDI-TOF.Conclusion: We suggested that TRAIL induces the apoptoticdeath of Chang cells via proteome alterations inducingcaspase cascade. (Cancer Res Treat. 2003;35:341-348)
So, Hong-Seob,Park, Channy,Kim, Hyung-Jin,Lee, Jung-Han,Park, Sung-Yeol,Lee, Jai-Hyung,Lee, Zee-Won,Kim, Hyung-Min,Kalinec, Federico,Lim, David J.,Park, Raekil Elsevier/North-Holland,Biomedical Press 2005 Hearing research Vol.204 No.1-2
<P><B>Abstract</B></P><P>Changes in intracellular Ca<SUP>2+</SUP> level are involved in a number of intracellular events, including triggering of apoptosis. The role of intracellular calcium mobilization in cisplatin-induced hair cell death, however, is still unknown. In this study, the effect of calcium channel blocker flunarizine (Sibelium™), which is used to prescribe for vertigo and tinnitus, on cisplatin-induced hair cell death was investigated in a cochlear organ of Corti-derived cell line, HEI-OC1, and the neonatal (P2) rat organ of Corti explant. Cisplatin induced apoptotic cell death showing nuclear fragmentation, DNA ladder, and TUNEL positive in both HEI-OC1 and primary organ of Corti explant. Flunarizine significantly inhibited the cisplatin-induced apoptosis. Unexpectedly, flunarizine increased the intracellular calcium ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) levels of HEI-OC1. However, the protective effect of flunarizine against cisplatin was not mediated by modulation of intracellular calcium level. Treatment of cisplatin resulted in ROS generation and lipid peroxidation in HEI-OC1. Flunarizine did not attenuate ROS production but inhibited lipid peroxidation and mitochondrial permeability transition in cisplatin-treated cells. This result suggests that the protective mechanism of flunarizine on cisplatin-induced cytotoxicity is associated with direct inhibition of lipid peroxidation and mitochondrial permeability transition.</P>
Role of proinflammatory cytokines in cisplatin-induced vestibular hair cell damage
Kim, Hyung-Jin,So, Hong-Seob,Lee, Jeong-Han,Park, Channy,Lee, Jin-Bin,Youn, Myung-Ja,Kim, Se-Jin,Yang, Sei-Hoon,Lee, Kang-Min,Kwon, Kang-Beom,Park, Byung-Hyun,Park, Raekil Wiley Subscription Services, Inc., A Wiley Company 2008 Head & neck Vol.30 No.11
<B>Background.</B><P>Cisplatin causes the impairment of inner ear functions, including hearing and balance, through the involvement of a number of mechanisms. However, no laboratory studies have been performed on involvement of inflammation-related events in cisplatin-mediated vestibular dysfunction.</P><B>Methods.</B><P>We evaluated the secretion of proinflammatory cytokines and nuclear factor-κB (NF-κB) activation in cisplatin-treated UB/UE-1 utricular epithelial cells. We also employed immunohistochemistry to detect proinflammatory cytokines and NF-κB expression in cisplatin-injected mice.</P><B>Results.</B><P>Productions of proinflammatory cytokines significantly caused the death of UB/UE1 cells by cisplatin. Pharmacologic inhibition of mitogen-activated protein (MAP) kinase/ERK kinase-1 (MEK1) or extracellular signal-regulated kinase (ERK) significantly attenuated the death of UB/UE1 cells caused by cisplatin and proinflammatory cytokines. Immunohistochemical studies revealed an increase in the expression of proinflammatory cytokines and NF-κB in both the cristae ampullae and utricle of cisplatin-injected mice.</P><B>Conclusions.</B><P>These results suggest that proinflammatory cytokines may play an important role in the pathogenesis of cisplatin-mediated vestibulotoxicity. © 2008 Wiley Periodicals, Inc. Head Neck, 2008</P>
Mitochondria-associated programmed cell death as a therapeutic target for age-related disease
Nguyen Thanh T.,Wei Shibo,Nguyen Thu Ha,Jo Yunju,Zhang Yan,Park Wonyoung,Gariani Karim,Oh Chang-Myung,Kim Hyeon Ho,Ha Ki-Tae,Park Kyu-Sang,Park Raekil,Lee In-Kyu,Shong Minho,Houtkooper Riekelt H.,Ryu 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Mitochondria, ubiquitous double-membrane-bound organelles, regulate energy production, support cellular activities, harbor metabolic pathways, and, paradoxically, mediate cell fate. Evidence has shown mitochondria as points of convergence for diverse cell death-inducing pathways that trigger the various mechanisms underlying apoptotic and nonapoptotic programmed cell death. Thus, dysfunctional cellular pathways eventually lead or contribute to various age-related diseases, such as neurodegenerative, cardiovascular and metabolic diseases. Thus, mitochondrion-associated programmed cell death-based treatments show great therapeutic potential, providing novel insights in clinical trials. This review discusses mitochondrial quality control networks with activity triggered by stimuli and that maintain cellular homeostasis via mitohormesis, the mitochondrial unfolded protein response, and mitophagy. The review also presents details on various forms of mitochondria-associated programmed cell death, including apoptosis, necroptosis, ferroptosis, pyroptosis, parthanatos, and paraptosis, and highlights their involvement in age-related disease pathogenesis, collectively suggesting therapeutic directions for further research.