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15 results on '"Lee, Sheau-Long"'

4. IgA Nephropathy Benefits from Compound K Treatment by Inhibiting NF-κB/NLRP3 Inflammasome and Enhancing Autophagy and SIRT1

Author

Wu, Chung-Yao, primary, Hua, Kuo-Feng, additional, Hsu, Wan-Han, additional, Suzuki, Yusuke, additional, Chu, Lichieh Julie, additional, Lee, Yu-Chieh, additional, Takahata, Akiko, additional, Lee, Sheau-Long, additional, Wu, Chia-Chao, additional, Nikolic-Paterson, David J., additional, Ka, Shuk-Man, additional, and Chen, Ann, additional

Published
2020
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5. Accelerated and Severe Lupus Nephritis Benefits From M1, an Active Metabolite of Ginsenoside, by Regulating NLRP3 Inflammasome and T Cell Functions in Mice

Author

Lin, Tsai-Jung, primary, Wu, Chung-Yao, additional, Tsai, Pei-Yi, additional, Hsu, Wan-Han, additional, Hua, Kuo-Feng, additional, Chu, Ching-Liang, additional, Lee, Yu-Chieh, additional, Chen, Ann, additional, Lee, Sheau-Long, additional, Lin, Yi-Jin, additional, Hsieh, Chih-Yu, additional, Yang, Shin-Ruen, additional, Liu, Feng-Cheng, additional, and Ka, Shuk-Man, additional

Published
2019
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6. Compound K inhibits priming and mitochondria-associated activating signals of NLRP3 inflammasome in renal tubulointerstitial lesions

Author

Hsu, Wan-Han, primary, Hua, Kuo-Feng, additional, Tuan, Li-Heng, additional, Tsai, Yu-Ling, additional, Chu, Lichieh Julie, additional, Lee, Yu-Chieh, additional, Wong, Wei-Ting, additional, Lee, Sheau-Long, additional, Lai, Jenn-Haung, additional, Chu, Ching-Liang, additional, Ho, Ling-Jun, additional, Chiu, Hsiao-Wen, additional, Hsu, Yu-Juei, additional, Chen, Cheng-Hsu, additional, Ka, Shuk-Man, additional, and Chen, Ann, additional

Published
2019
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7. Compound K inhibits priming and mitochondria-associated activating signals of NLRP3 inflammasome in renal tubulointerstitial lesions.

Author

Hsu, Wan-Han, Hua, Kuo-Feng, Tuan, Li-Heng, Tsai, Yu-Ling, Chu, Lichieh Julie, Lee, Yu-Chieh, Wong, Wei-Ting, Lee, Sheau-Long, Lai, Jenn-Haung, Chu, Ching-Liang, Ho, Ling-Jun, Chiu, Hsiao-Wen, Hsu, Yu-Juei, Chen, Cheng-Hsu, Ka, Shuk-Man, and Chen, Ann

Subjects
NLRP3 protein, MONONUCLEAR leukocytes, RENAL fibrosis, CHRONIC kidney failure, TREATMENT effectiveness, EPITHELIAL cells
Abstract

Background Renal tubulointerstitial lesions (TILs), a key pathological hallmark for chronic kidney disease to progress to end-stage renal disease, feature renal tubular atrophy, interstitial mononuclear leukocyte infiltration and fibrosis in the kidney. Our study tested the renoprotective and therapeutic effects of compound K (CK), as described in our US patent (US7932057B2), on renal TILs using a mouse unilateral ureteral obstruction (UUO) model. Methods Renal pathology was performed and renal draining lymph nodes were subjected to flow cytometry analysis. Mechanism-based experiments included the analysis of mitochondrial dysfunction, a model of tubular epithelial cells (TECs) under mechanically induced constant pressure (MICP) and tandem mass tags (TMT)-based proteomics analysis. Results Administration of CK ameliorated renal TILs by reducing urine levels of proinflammatory cytokines, and preventing mononuclear leukocyte infiltration and fibrosis in the kidney. The beneficial effects clearly correlated with its inhibition of: (i) NF-κB-associated priming and the mitochondria-associated activating signals of the NLRP3 inflammasome; (ii) STAT3 signalling, which in part prevents NLRP3 inflammasome activation; and (iii) the TGF-β-dependent Smad2/Smad3 fibrotic pathway, in renal tissues, renal TECs under MICP and/or activated macrophages, the latter as a major inflammatory player contributing to renal TILs. Meanwhile, TMT-based proteomics analysis revealed downregulated renal NLRP3 inflammasome activation-associated signalling pathways in CK-treated UUO mice. Conclusions The present study, for the first time, presents the potent renoprotective and therapeutic effects of CK on renal TILs by targeting the NLRP3 inflammasome and STAT3 signalling. [ABSTRACT FROM AUTHOR]

Published
2020
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14. Ginsenoside compound K reduces the progression of Huntington's disease via the inhibition of oxidative stress and overactivation of the ATM/AMPK pathway

Author

Hua, Kuo-Feng, Chao, A-Ching, Lin, Ting-Yu, Chen, Wan-Tze, Lee, Yu-Chieh, Hsu, Wan-Han, Lee, Sheau-Long, Wang, Hsin-Min, Yang, Ding-I., and Ju, Tz-Chuen

Abstract

Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion of trinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HD involve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinase ataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM is involved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays a critical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expanded mutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effective component of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HD remains unclear and warrants further investigation.

Published
2021
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