KMID : 0363320190400030425
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Journal of Korean Oriental Internal Medicine 2019 Volume.40 No. 3 p.425 ~ p.442
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Pharmacological Properties of CDBT in Hypoxia-induced Neuronal Cell Injury and Their Underlying Mechanisms
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Park Sang-Kyu
Jung Eun-Sun Cha Ji-Yoon Cho Hyun-Kyoung Yoo Ho-Ryong Kim Yoon-Sik Seol In-Chan
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Abstract
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Objectives: This study aimed to reveal the pharmacological properties of the newly prescribed herbal mixture, Chenmadansam- gamibokhap-tang (CDBT), against hypoxia-induced neuronal cell injury (especially mouse hippocampal neuronal cell line, HT-22 cells) and their corresponding mechanisms.
Methods: A cell-based in vitro experiment, in which a hypoxia condition induced neuronal cell death, was performed. Various concentrations of the CDBT were pre-treated to the HT-22 cells for 4 h before 18 h in the hypoxia chamber. The glial cell BV-2 cells were stimulated with IFN¥ã and LSP to produce inflammatory cytokines and reactive oxygen species. When the neuronal HT-22 cells were treated with this culture solution, the drug efficacy against neuronal cell death was examined.
Results: CDBT showed cytotoxicity in the normal condition of HT-22 cells at a dose of 125 ¥ìg/mL and showed a protective
effect against hypoxia-induced neuronal cell death at a dose of 31.3 ¥ìg/mL. CDBT prevented hypoxia-induced neuronal cell death in a dose-dependent manner in the HT-22 cells by regulating HIF1¥á and cell death signaling. CDBT prevented neuronal cell death signals and DNA fragmentation due to the hypoxia condition. CDBT significantly reduced cellular oxidation, cell death signals, and caspase-3 activities due to microglial cell activations. Moreover, CDBT significantly ameliorated LPS-induced BV-2 cell activation and evoked cellular oxidation through the recovery of redox homeostasis.
Conclusions: CDBT cam be considered as a vital therapeutic agent against neuronal cell deaths. Further studies are required to reveal the other functions of CDBT in vivo or in the clinical field.
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KEYWORD
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herbal medicine, hypoxia, cell death, neuronal oxidation, HT-22 cells
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