American ginseng significantly reduced the progression of high-fat-diet-enhanced colon carcinogenesis in Apc^Min/+ mice

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.

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.

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.

Loss of MicroRNA-137 Impairs the Homeostasis of Potassium in Neurons via KCC2

Ting-Wei Mi,Xiao-Wen Sun,Zhi-Meng Wang,Ying-Ying Wang,Xuan-Cheng He,Cong Liu,Shuang-Feng Zhang,Hong-Zhen Du,Chang-Mei Liu,Zhao-Qian Teng 한국뇌신경과학회 2020 Experimental Neurobiology Vol.29 No.2

Neuropsychiatric disorders are the leading cause of mental and intellectual disabilities worldwide. Current therapies against neuropsychiatric disorders are very limited, and very little is known about the onset and development of these diseases, and their most effective treatments. MIR137 has been previously identified as a risk gene for the etiology of schizophrenia, bipolar disorder, and autism spectrum disorder. Here we generated a forebrain-specific MIR137 knockout mouse model, and provided evidence that loss of miR-137 resulted in impaired homeostasis of potassium in mouse hippocampal neurons. KCC2, a potassium-chloride co-transporter, was a direct downstream target of miR-137. The KCC2 specific antagonist VU0240551 could balance the current of potassium in miR-137 knockout neurons, and knockdown of KCC2 could ameliorate anxiety-like behavior in MIR137 cKO mice. These data suggest that KCC2 antagonists or knockdown might be beneficial to neuropsychiatric disorders due to the deficiency of miR-137.

Dynamic analysis for gene expression profiles of endothelial colony forming cells under hypoxia

De-Cai Yu,Wen-Du Feng,Xian-Biao Shi,hi-Yong Wang,Wei Ge,Chun-Ping Jiang,Xi-Tai Sun,Yi-Tao Ding 한국유전학회 2013 Genes & Genomics Vol.35 No.4

Previous studies have shown that endothelial colony forming cells (ECFCs) play an important role in the neovascularization of tumors. Hypoxia is emphasized as an important promoter of angiogenesis. However, little is known about genome-wide transcriptional regulation of ECFCs under hypoxic conditions. In this study, gene expression profiles in ECFCswere evaluated under hypoxic conditions for 3, 6, 12, 24,and 48 h, using Affymetrix U133 plus 2.0 chip microarray. 1,103 hypoxia-regulated genes were filtered, with 379(0.693 %) genes up-regulated and 724 (1.32 %) genes downregulated. Most of the up-regulated genes were involved in apoptosis, cell proliferation, or metabolic processes, while most of the down-regulated genes were involved in cell adherence,cell cycle,DNAandmRNAmetabolic processes,multi-cellular organism development, protein metabolic processes, response to stress, signal transduction, or transport. This expression profile is ECFC-specific, because it is significantly different from those of endothelial cells and smooth muscle cells under hypoxic conditions. Moreover, hypoxia-regulated apoptosis in ECFCs is mainly related with the mitochondrial pathway (p53-BAX-Caspase-9) and the death receptor pathway (FASCaspase-8-Caspase-3). MAPK pathway is activated in ECFCs under hypoxic conditions. The differentially expressed genes of ECFCs were identified under hypoxic conditions, and related with cell apoptosis, cell cycle and MAPK pathways, shedding light on the mechanism of angiogenesis.

American ginseng significantly reduced the progression of high-fatdiet-enhanced colon carcinogenesis in ApcMin/þmice

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.

Crocetin Induces Cytotoxicity in Colon Cancer Cells Via p53-independent Mechanisms

Li, Cai-Yan,Huang, Wen-Feng,Wang, Qun-Li,Wang, Fan,Cai, E.,Hu, Bing,Du, Jia-Cheng,Wang, Jing,Chen, Rong,Cai, Xiao-Jing,Feng, Jing,Li, Hui-Hui Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.8

Objective: Crocin has been proposed as a promising candidate for cancer chemoprevention. The purpose of this investigation was to investigate the chemopreventive action and the possible mechanisms of crocin against human colon cancer cells in vitro. Methods: Cell proliferation was examined using MTT assay and the cell cycle distribution fractions were analyzed using fow cytometric analysis after propidium iodide staining. Apoptosis was detected using theTUNEL Apoptosis Detection Kit with laser scanning confocal microscope. DNA damage was assessed using the alkaline single-cell gel electrophoresis assay, while expression levels of p53, cdk2, cyclinA and P21 were examined by Western blot analysis. Results: Treatment of SW480 cells with crocetin (0.2, 0.4, 0.8 mmol/L) for 48 h signifcantly inhibited their proliferation in a concentration-dependent manner. Crocetin (0.8 mmol/L) signifcantly induced cell cycle arrest through p53-independent mechanisms accompanied by P21 induction. Crocetin (0.8 mmol/L) caused cytotoxicity in the SW480 cells by enhancing apoptosis and decreasing DNA repair capacity in a time-dependent manner. Conclusions: This report provides evidence that crocetin is a potential anticancer agent, which may be used as a chemotherapeutic drug.

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.

Post-fire Study on Mechanical Properties of Damaged Ultra-high Strength Concrete

Xiao Lyu,Guang-Hao Jia,Gan-Ping Shu,Xin Zhang,Er-Feng Du,Wen-Ming Wang 한국강구조학회 2022 International Journal of Steel Structures Vol.22 No.6

In order to study the eff ect of steel tube, pre-load and temperature on residual performance of heated ultra-high strength concrete (UHSC), an experimental program was carried out to investigate the physical and mechanical properties of UHSC post-fi re in room temperature. With total of 54 standard cylindrical concrete specimens subjected to various temperatures ranging from 62 °C to 496 °C, their residual compressive strength, elastic modulus, peak strain was measured after natural cooling down. By comparing the test results of standard cylindrical concrete specimens with the results of the bare specimens in and after fi re, it is known that the residual compressive strength of standard cylindrical concrete specimens decayed more serious after exposing to same temperature. Seen from the results, the temperature which the specimens suff ered was found to be responsibility to the reduction of the compressive strength, elastic modulus, peak strain. As the temperature up to 300 °C, the strength reduction coeffi cient of UHSC was 0.67 ~ 0.68 and the elastic modulus reduction coeffi cient of UHSC was 0.41 ~ 0.51 with peak strain coeffi cient ε cr ( T ) /ε 0 1.57 ~ 1.67. Finally, based on the analysis of test results, simple formulae were proposed to describe the eff ect of temperature on residual performance of heated UHSC which infi lled the steel tube.

A New Hybrid Active Noise Control System: Adaptive Plant Disturbance Canceling Structure Combined with Narrowband Adaptive Noise Canceling Structure

Shan-zhen Yi,Ren-yuan Fei,Da-sen Zhou,Zhong-ting Dou,Feng-guang Zhou,Ya-du Sun,Qing-lin Wen 한국소음진동공학회 2003 한국소음진동공학회 국제학술대회논문집 Vol.2003 No.8