• Title/Summary/Keyword: colonic cells apoptosis

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The Effects of Coicis Semen Extract (CSE) on Dextran Sulfate Sodium - Induced Colitis in Mice (의이인(薏苡仁) 추출물이 DSS(dextran sulfate sodium)로 유발된 생쥐의 궤양성 대장염에 미치는 영향)

  • Heo, Gyeong;Jang, Myeong-Woong;Lim, Seong-Woo
    • The Journal of Internal Korean Medicine
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    • v.33 no.4
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    • pp.520-532
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    • 2012
  • Objectives : This study was carried out to investigate the effects of Coicis Semen Extract (CSE) on the experimental colitis induced by dextran sulfate sodium (DSS) in mice. Methods : Experimental colitis was induced by daily treatment with 5% DSS in the drinking water for 7 days in 6-week-old male ICR mice. The colitic mice were divided into three groups: the normal (N) group consisted of mice that were not inflammation-induced. The control (C) group was composed of untreated colitis elicited mice. The sample (S) group was administered CSE after colitis elicitation. The effects on colonic mucosal ulcers were evaluated by the morphological, histological and immunohistochemical change of the large intestine. Results : Inhibition of LPS-induced NO decreased in the S group. Inhibition of LPS-induced iNOS and COX-2 mRNA noticeably decreased in the S group from 0.25 mg/ml. In the common morphological and histochemical change, the erosion and the infiltration of inflammatory cells increased in the C group, while they noticeably decreased in the S group. The length of colon was shortened more in the C group than in the S group. The distributions of MUC2 and Hsp70 treated with CSE increased noticeably more in the S group than in the C group (p<0.05). It was confirmed histochemically and immunohistochemically that the distributions of iNOS, COX-2, MAC387, serotonin, apoptosis and PCNA treated with CSE decreased in the S group more than in the C group (p<0.05). Conclusions : It is confirmed that CSE has cytoprotective effect, so can alleviate inflammation process. Therefore, it is expected to have potential protective effect on colitis.

Structural Maintenance of Chromosomes 4 is a Predictor of Survival and a Novel Therapeutic Target in Colorectal Cancer

  • Feng, Xiao-Dong;Song, Qi;Li, Chuan-Wei;Chen, Jian;Tang, Hua-Mei;Peng, Zhi-Hai;Wang, Xue-Chun
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.21
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    • pp.9459-9465
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    • 2014
  • Background: Structural maintenance of chromosomes 4 (SMC-4) is a chromosomal ATPase which plays an important role in regulate chromosome assembly and segregation. However, the role of SMC-4 in the incidence of malignancies, especially colorectal cancer is still poorly understood. Materials and Methods: We here used quantitative PCR and Western blot analysis to examine SMC-4 mRNA and protein levels in primary colorectal cancer and paired normal colonic mucosa. SMC-4 clinicopathological significance was assessed by immunohistochemical staining in a tissue microarray (TMA) in which 118 cases of primary colorectal cancer were paired with noncancerous tissue. The biological function of SMC-4 knockdown was measured by CCK8 and plate colony formation assays. Fluorescence detection has been used to detect cell cycling and apoptosis. Results: SMC-4 expression was significantly higher in colorectal cancer and associated with T stage, N stage, AJCC stage and differentiation. Knockdown of SMC-4 expression significantly suppressed the proliferation of cancer cells and degraded its malignant degree. Conclusions: Our clinical and experimental data suggest that SMC-4 may contribute to the progression of colorectal carcinogenesis. Our study provides a new therapeutic target for colorectal cancer treatment.

Effect of Dietary Selenium on the Colon Carcinogenesis in Male ICR Mice

  • Cho, Min-Haeng;Kim, Jun-Hyeong;Hue, Jin-Joo;Kang, Bong-Su;Park, Hyun-Ji;Nam, Sang-Yoon;Yun, Young-Won;Kim, Jong-Soo;Jeong, Jae-Hwang;Lee, Beom-Jun
    • Journal of Food Hygiene and Safety
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    • v.25 no.3
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    • pp.269-277
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    • 2010
  • Selenium is an essential micronutrient for normal body function and functions as an essential constituent of selenoproteins. This study was carried out to investigate effect of selenium on the formation of colonic aberrant crypt foci (ACF) and tumor formation in a mouse model. Five-week old ICR mice were acclimated for one week and fed different selenium diet (0.02, 0.1, and 0.5 ppm) for 12 weeks. Animals received three intraperitoneal injections of azoxymethane (10 mg/kg B.W. in saline for 3 weeks), followed by 2% dextran sodium sulfate in the drinking water for a week. There were four experimental groups, including a normal control group and three different selenium levels groups. After sacrifice, the total numbers of aberrant crypt (AC) and ACF were measured in the colonic mucosa after methylene blue staining. The number of tumors was noted for tumor incidence. Liver selenium concentration was measured using ICP-AES method. Gutathione peroxidase (GPx) activity was determined using a GPx assay kit in the liver and colon. TUNEL assay and proliferating cell nuclear antigen (PCNA) staining were performed to examine the cell apoptosis and cell proliferation, respectively. Immunohistochemistry of $\beta$-catenin was also performed on the mucous membrane tissue of colon. The activity of GPx in the liver and colon was decreased in the selenium-deficient diet group while it was increased in the selenium-overloaded diet group. Apoptotic positive cells were increased in the selenium-overloaded diet group but decreased in the selenium-deficient diet group. PCNA staining area was decreased in the selenium-overloaded diet group. In addition, the $\beta$-catenin protein level in the selenium-deficient diet group was increased but decreased in the selenium-overloaded diet group. These results indicate that dietary selenium might exert a modulating effect on colon cancer by inhibiting the development of ACF and colon tumor formation in this mouse model.