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1,468 results on '"Han, Sang-Bae"'

166. Green Tea (-)-epigallocatechin-3-gallate inhibits [beta]-amyloid-induced cognitive dysfunction through modification of secretase activity via inhibition of ERK and NF-[kappa]B pathways in mice

Author

Lee, Jae Woong, Lee, Yong Kyoung, Ban, Jung Ok, Ha, Tae Youl, Yun, Yeo Pyo, Han, Sang Bae, Oh, Ki Wan, and Hong, Jin Tae

Subjects
Green tea -- Health aspects, Alzheimer's disease -- Care and treatment, Catechin -- Research, Food/cooking/nutrition
Abstract

Alzheimer's disease (AD) is characterized by the extracellular deposition of [beta]-amyloid peptide (A[beta]) in cerebral plaques. A[beta] is derived from the [beta]-amyloid precursor protein (APP) by the enzymes [alpha]-,[beta]- and [gamma]-secretase. Compounds that enhance [alpha]-secretase, but inhibit [beta]- or [gamma]-secretase activity, have therapeutic potential in the treatment of AD. Green tea, or its major polyphenolic compound, has been shown to have neuroprotective effects. In this study, we investigated the possible effects of (-)-epigallocatechin-3-gallate (EGCG) on memory dysfunction caused by A[beta] through the change of A[beta]-induced secretase activities. Mice were pretreated with EGCG (1.5 or 3 mg/kg body weight in drinking water) for 3 wk before intracerebroventricular administration of 0.5 [micro]g A[[beta].sub.1-42]. EGCG dose-dependently reduced the A[[beta].sub.1-42]-induced memory dysfunction, which was evaluated using passive avoidance and water maze tests. A[[beta].sub.1-42] induced a decrease in brain [alpha]-secretase and increases in both brain [beta]- and [gamma]-secretase activities, which were reduced by EGCG. In the cortex and the hippocampus, expression of the metabolic products of the [beta]- and [gamma]-secretases from APP, C99, and A[beta] also were dose-dependently suppressed by EGCG. Paralleled with the suppression of [beta]- and [gamma]-secretases by EGCG, we found that EGCG inhibited the activation of extracellular signal-regulated kinase and nuclear transcription factor-[kappa]B in the A[[beta].sub.1-42]-injected mouse brains. In addition, EGCG inhibited A[[beta].sub.1-42]-induced apoptotic neuronal cell death in the brain. To further test the ability of EGCG to affect memory, EGCG (3 mg/kg body weight) was administered in drinking water for 1 wk to genetically developed preseniline 2 (PS2) mutant AD mice. Compared with untreated mutant PS2 AD mice, treatment with EGCG enhanced memory function and brain [alpha]-secretase activity but reduced brain [beta]- and [gamma]-secretase activities as well as A[beta] levels. Moreover, EGCG inhibited the fibrillization of A[beta] in vitro with a half maximal inhibitory concentration of 7.5 mg/L. These studies suggest that EGCG may be a beneficial agent in the prevention of development or progression of AD.

Published
2009

169. Novel 4-Oxoquinazoline-Based N-Hydroxypropenamides as Histone Deacetylase Inhibitors: Design, Synthesis, and Biological Evaluation

Author

Anh, Duong T., primary, Hai, Pham-The, additional, Huy, Le D., additional, Ngoc, Hoang B., additional, Ngoc, Trinh T. M., additional, Dung, Do T. M., additional, Park, Eun J., additional, Song, In K., additional, Kang, Jong S., additional, Kwon, Joo-Hee, additional, Tung, Truong T., additional, Han, Sang-Bae, additional, and Nam, Nguyen-Hai, additional

Published
2021
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188. A small molecule targeting CHI3L1 inhibits lung metastasis by blocking IL‐13Rα2‐mediated JNK‐AP‐1 signals.

Author

Lee, Yong Sun, Yu, Ji Eun, Kim, Ki Cheon, Lee, Dong Hun, Son, Dong Ju, Lee, Hee Pom, Jung, Jae‐kyung, Kim, Nam Du, Ham, Young Wan, Yun, Jaesuk, Han, Sang‐Bae, and Hong, Jin Tae

Abstract

Our previous big data analyses showed a high level of association between chitinase 3 like1 (CHI3L1) expression and lung tumor development. In the present study, we investigated whether a CHI3L1‐inhibiting chemical, 2‐({3‐[2‐(1‐cyclohexen‐1‐yl)ethyl]‐6,7‐dimethoxy‐4‐oxo‐3,4‐dihydro‐2‐quinazolinyl}sulfanyl)‐N‐(4‐ethylphenyl)butanamide (K284), could inhibit lung metastasis and studied its mechanism of action. We investigated the antitumor effect of K284 both in vitro and in vivo. K284 (0.5 mg·kg−1 body weight) significantly inhibited lung metastasis in in vivo models after injection of murine melanoma cells (B16F10) or adenocarcinomic human alveolar basal epithelial cells (A549). K284 significantly and concentration‐dependently also inhibited cancer cell proliferation and migration in the A549 and H460 lung cancer cell lines. We found that the binding of K284 to the chitin‐binding domain (CBD) of CHI3L1 prevented the binding of CHI3L1 to its receptor, interleukin‐13 receptor subunit alpha‐2 (IL‐13Rα2), thereby suppressing the CHI3L1 signal. This blocking of the CHI3L1‐IL‐13Rα2 signal caused the inhibition of c‐Jun N‐terminal kinase (JNK)‐activator protein 1 (AP‐1) signals, resulting in the prevention of lung metastasis and cancer cell growth. Our data demonstrate that K284 may serve as a potential candidate anticancer compound targeting CHI3L1. [ABSTRACT FROM AUTHOR]

Published
2022
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