1.A stochastic analysis on the force of infection by hepatitis B virus in Korea.
Keun Young YOO ; Moo Song LEE ; Youngjo LEE ; Bo Youl CHOI ; Heon KIM ; Yong Sik KIM
Korean Journal of Epidemiology 1992;14(2):128-137
No abstract available.
Hepatitis B virus*
;
Hepatitis B*
;
Hepatitis*
;
Korea*
2.Rutaecarpine, Isolated from Evodia rutaecarpa, Inhibits Epithelial-Mesenchymal Transition and Cellular Senescence in a Mouse Model of Pulmonary Fibrosis
Eun CHOI ; Yeseul CHO ; Misu KIM ; Hee JIN ; Youngjo YOO ; Won Keun OH ; Yun-sil LEE
Natural Product Sciences 2024;30(3):190-197
Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.
3.Rutaecarpine, Isolated from Evodia rutaecarpa, Inhibits Epithelial-Mesenchymal Transition and Cellular Senescence in a Mouse Model of Pulmonary Fibrosis
Eun CHOI ; Yeseul CHO ; Misu KIM ; Hee JIN ; Youngjo YOO ; Won Keun OH ; Yun-sil LEE
Natural Product Sciences 2024;30(3):190-197
Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.
4.Rutaecarpine, Isolated from Evodia rutaecarpa, Inhibits Epithelial-Mesenchymal Transition and Cellular Senescence in a Mouse Model of Pulmonary Fibrosis
Eun CHOI ; Yeseul CHO ; Misu KIM ; Hee JIN ; Youngjo YOO ; Won Keun OH ; Yun-sil LEE
Natural Product Sciences 2024;30(3):190-197
Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.
5.Rutaecarpine, Isolated from Evodia rutaecarpa, Inhibits Epithelial-Mesenchymal Transition and Cellular Senescence in a Mouse Model of Pulmonary Fibrosis
Eun CHOI ; Yeseul CHO ; Misu KIM ; Hee JIN ; Youngjo YOO ; Won Keun OH ; Yun-sil LEE
Natural Product Sciences 2024;30(3):190-197
Cellular senescence, a type of cytostasis, is the irreversible inhibition of the natural cell division in proliferating cells, resulting from various cellular stresses, including telomere shortening, DNA damage, mitochondrial dysfunctions, and pro-inflammatory responses. While cellular senescence can facilitate beneficial physiological processes such as tissue repair and wound healing, senescent cells also contribute to pathophysiological processes of agerelated diseases, including fibrotic lung diseases. The cellular senescence model and co-culture system were established to explore the underlying mechanisms associated with cellular senescence and fibrosis. Rutaecarpine is a bioactive alkaloid isolated from Evodia rutaecarpa (Rutaceae), a traditional herbal medicine. Rutaecarpine enhanced the promotor activity of E-cadherin, reduced TGF-β-induced reorganization of the actin cytoskeleton, and finally inhibited epithelialmesenchymal transition. Rutaecarpine also attenuated fibrotic and senescence features in bleomycin-induced lung fibrosis model. Here, we suggest the relevance between senescence and fibrosis, and a potential therapeutic approach of targeting senescence to attenuate lung fibrosis development.