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RISS 인기검색어
- 검색키워드
- 저자 : ( Tong-chuan He ) (검색결과 7 건)
- 무료
- 기관 내 무료
- 유료
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Yu, Chunhao,Wen, Xiao-Dong,Zhang, Zhiyu,Zhang, Chun-Feng,Wu, Xiaohui,He, Xin,Liao, Yang,Wu, Ningning,Wang, Chong-Zhi,Du, Wei,He, Tong-Chuan,Yuan, Chun-Su The Korean Society of Ginseng 2015 Journal of Ginseng Research Vol.39 No.3
Background: Colorectal cancer (CRC) is a leading cause of death worldwide. Chronic gut inflammation is recognized as a risk factor for tumor development, including CRC. American ginseng is a very commonly used ginseng species in the West. Methods: A genetically engineered $Apc^{Min/+}$ mouse model was used in this study. We analyzed the saponin composition of American ginseng used in this project, and evaluated its effects on the progression of high-fat-diet-enhanced CRC carcinogenesis. Results: After oral ginseng administration (10-20 mg/kg/d for up to 32 wk), experimental data showed that, compared with the untreated mice, ginseng very significantly reduced tumor initiation and progression in both the small intestine (including the proximal end, middle end, and distal end) and the colon (all p < 0.01). This tumor number reduction was more obvious in those mice treated with a low dose of ginseng. The tumor multiplicity data were supported by body weight changes and gut tissue histology examinations. In addition, quantitative real-time polymerase chain reaction analysis showed that compared with the untreated group, ginseng very significantly reduced the gene expression of inflammatory cytokines, including interleukin-$1{\alpha}$ (IL-$1{\alpha}$), IL-$1{\beta}$, IL-6, tumor necrosis factor-${\alpha}$, granulocyte-colony stimulating factor, and granulocyte-macrophage colony-stimulating factor in both the small intestine and the colon (all p < 0.01). Conclusion: Further studies are needed to link our observed effects to the actions of the gut microbiome in converting the parent ginsenosides to bioactive ginseng metabolites. Our data suggest that American ginseng may have potential value in CRC chemoprevention.
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Chunhao Yu,Xiao-Dong Wen,Zhiyu Zhang,Chun-Feng Zhang,Xiaohui Wu,Xin He,Yang Liao,Ningning Wu,Chong-Zhi Wang,Wei Du,Tong-Chuan He,Chun-Su Yuan 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.3
Background: Colorectal cancer (CRC) is a leading cause of death worldwide. Chronic gut inflammation is recognized as a risk factor for tumor development, including CRC. American ginseng is a very commonly used ginseng species in the West. Methods: A genetically engineered ApcMin/þ mouse model was used in this study. We analyzed the saponin composition of American ginseng used in this project, and evaluated its effects on the progression of high-fat-diet-enhanced CRC carcinogenesis. Results: After oral ginseng administration (10e20 mg/kg/d for up to 32 wk), experimental data showed that, compared with the untreated mice, ginseng very significantly reduced tumor initiation and progression in both the small intestine (including the proximal end, middle end, and distal end) and the colon (all p < 0.01). This tumor number reduction was more obvious in those mice treated with a low dose of ginseng. The tumor multiplicity data were supported by body weight changes and gut tissue histology examinations. In addition, quantitative real-time polymerase chain reaction analysis showed that compared with the untreated group, ginseng very significantly reduced the gene expression of inflammatory cytokines, including interleukin-1a (IL-1a), IL-1b, IL-6, tumor necrosis factor-a, granulocyte-colony stimulating factor, and granulocyte-macrophage colony-stimulating factor in both the small intestine and the colon (all p < 0.01). Conclusion: Further studies are needed to link our observed effects to the actions of the gut microbiome in converting the parent ginsenosides to bioactive ginseng metabolites. Our data suggest that American ginseng may have potential value in CRC chemoprevention.
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American ginseng attenuates azoxymethane/dextran sodium sulfate-induced colon carcinogenesis in mice
Yu, Chunhao,Wen, Xiao-Dong,Zhang, Zhiyu,Zhang, Chun-Feng,Wu, Xiao-Hui,Martin, Adiba,Du, Wei,He, Tong-Chuan,Wang, Chong-Zhi,Yuan, Chun-Su The Korean Society of Ginseng 2015 Journal of Ginseng Research Vol.39 No.1
Background: Colorectal cancer is a leading cause of cancer-related death, and inflammatory bowel disease is a risk factor for this malignancy. We previously reported colon cancer chemoprevention potential using American ginseng (AG) in a xenograft mice model. However, the nude mouse model is not a gut-specific colon carcinogenesis animal model. Methods: In this study, an experimental colitis and colitis-associated colorectal carcinogenesis mouse model, chemically induced by azoxymethane/dextran sodium sulfate (DSS) was established and the effects of oral AG were evaluated. The contents of representative ginseng saponins in the extract were determined. Results: AG significantly reduced experimental colitis measured by the disease activity index scores. This suppression of the experimental colitis was not only evident during DSS treatment, but also very obvious after the cessation of DSS, suggesting that the ginseng significantly promoted recovery from the colitis. Consistent with the anti-inflammation data, we showed that ginseng very significantly attenuated azoxymethane/DSS-induced colon carcinogenesis by reducing the colon tumor number and tumor load. The ginseng also effectively suppressed DSS-induced proinflammatory cytokines activation using an enzyme-linked immunosorbent assay array, in which 12 proinflammatory cytokine levels were assessed, and this effect was supported subsequently by real-time polymerase chain reaction data. Conclusion: AG, as a candidate of botanical-based colon cancer chemoprevention, should be further investigated for its potential clinical utility.
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American ginseng attenuates azoxymethane/dextran sodium sulfate-induced colon carcinogenesis in mice
Chunhao Yu,Xiao-Dong Wen,Zhiyu Zhang,Chun-Feng Zhang,Xiao-Hui Wu,Adiba Martin,Wei Du,Tong-Chuan He,Chong-Zhi Wang,Chun-Su Yuan 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.3
Background: Colorectal cancer is a leading cause of cancer-related death, and inflammatory bowel disease is a risk factor for this malignancy. We previously reported colon cancer chemoprevention potential using American ginseng (AG) in a xenograft mice model. However, the nude mouse model is not a gutspecific colon carcinogenesis animal model. Methods: In this study, an experimental colitis and colitis-associated colorectal carcinogenesis mouse model, chemically induced by azoxymethane/dextran sodium sulfate (DSS) was established and the effects of oral AG were evaluated. The contents of representative ginseng saponins in the extract were determined. Results: AG significantly reduced experimental colitis measured by the disease activity index scores. This suppression of the experimental colitis was not only evident during DSS treatment, but also very obvious after the cessation of DSS, suggesting that the ginseng significantly promoted recovery from the colitis. Consistent with the anti-inflammation data, we showed that ginseng very significantly attenuated azoxymethane/DSS-induced colon carcinogenesis by reducing the colon tumor number and tumor load. The ginseng also effectively suppressed DSS-induced proinflammatory cytokines activation using an enzyme-linked immunosorbent assay array, in which 12 proinflammatory cytokine levels were assessed, and this effect was supported subsequently by real-time polymerase chain reaction data. Conclusion: AG, as a candidate of botanical-based colon cancer chemoprevention, should be further investigated for its potential clinical utility.
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American ginseng attenuates azoxymethane/dextran sodium sulfate-induced colon carcinogenesis in mice
Chunhao Yu,Xiao-Dong Wen,Zhiyu Zhang,Chun-Feng Zhang,Xiao-Hui Wu,Adiba Martin,Wei Du,Tong-Chuan He,Chong-Zhi Wang,Chun-Su Yuan 고려인삼학회 2015 Journal of Ginseng Research Vol.39 No.1
Background: Colorectal cancer is a leading cause of cancer-related death, and inflammatory bowel diseaseis a risk factor for this malignancy. We previously reported colon cancer chemoprevention potentialusing American ginseng (AG) in a xenograft mice model. However, the nude mouse model is not a gutspecificcolon carcinogenesis animal model. Methods: In this study, an experimental colitis and colitis-associated colorectal carcinogenesis mousemodel, chemically induced by azoxymethane/dextran sodium sulfate (DSS) was established and theeffects of oral AG were evaluated. The contents of representative ginseng saponins in the extract weredetermined. Results: AG significantly reduced experimental colitis measured by the disease activity index scores. Thissuppression of the experimental colitis was not only evident during DSS treatment, but also very obviousafter the cessation of DSS, suggesting that the ginseng significantly promoted recovery from the colitis. Consistent with the anti-inflammation data, we showed that ginseng very significantly attenuatedazoxymethane/DSS-induced colon carcinogenesis by reducing the colon tumor number and tumor load. The ginseng also effectively suppressed DSS-induced proinflammatory cytokines activation using anenzyme-linked immunosorbent assay array, in which 12 proinflammatory cytokine levels were assessed,and this effect was supported subsequently by real-time polymerase chain reaction data. Conclusion: AG, as a candidate of botanical-based colon cancer chemoprevention, should be furtherinvestigated for its potential clinical utility.
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Biphasic effects of TGFβ1 on BMP9-induced osteogenic differentiation of mesenchymal stem cells
( Rui Dong Li ),( Zhong Liang Deng ),( Ning Hu ),( Xi Liang ),( Bo Liu ),( Jin Yong Luo ),( Liang Chen ),( Liang Jun Yin ),( Xiao Ji Luo ),( Wei Shui ),( Tong Chuan He ),( Wei Huang ) 생화학분자생물학회(구 한국생화학분자생물학회) 2012 BMB Reports Vol.45 No.9
We have found that the previously uncharacterized bone morphogenetic protein-9 (BMP9) is one of the most osteogenic factors. However, it is unclear if BMP9 cross-talks with TGFβ1 during osteogenic differentiation. Using the recombinant BMP9 adenovirus, we find that low concentration of rhTGFβ1 synergistically induces alkaline phosphatase activity in BMP9-transduced C3H10T1/2 cells and produces more pronounced matrix mineralization. However, higher concentrations of TGFβ1 inhibit BMP9-induced osteogenic activity. Real-time PCR and Western blotting indicate that BMP9 in combination with low dose of TGFβ1 potentiates the expression of later osteogenic markers osteopontin, osteocalcin and collagen type 1 (COL1a2), while higher concentrations of TGFβ1 decrease the expression of osteopontin and osteocalcin but not COL1a2. Cell cycle analysis reveals that TGFβ1 inhibits C3H10T1/2 proliferation in BMP9-induced osteogenesis and restricts the cells in G0/G1 phase. Our findings strongly suggest that TGFβ1 may exert a biphasic effect on BMP9-induced osteogenic differentiation of mesenchymal stem cells. [BMB Reports 2012; 45(9): 509-514]
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