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Expression of Heat Shock Proteins and Cytokines in Response to Ethanol Induced Damage in the Small Intestine of ICR Mice
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Sung Won Lee, Dong Wook Choi, Sung Chul Park, Hee Jung Kim, Yang Hoon Nam, Dae Hee Choi, Chang Don Kang, Sung Joon Lee, Wan Joo Chun, Young-Joon Ryu
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Intest Res 2014;12(3):205-213. Published online July 25, 2014
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DOI: https://doi.org/10.5217/ir.2014.12.3.205
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 Abstract
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- <b>Background/Aims</b><br/>
Ethanol administration causes intestinal epithelial cell damage by increasing intestinal permeability and the translocation of endotoxins from intestinal bacterial flora. Heat shock proteins (HSPs) are associated with recovery and protection from cell damage. The aim of the current study was to investigate differences in the expression of HSPs in the small intestine and the biochemical changes attributable to ethanol-induced intestinal damage. MethodsEthanol (20%) was injected intraperitoneally (2.75 g/kg, 5.5 g/kg, 8.25 g/kg) in ICR mice and the same volume of saline was administered to controls. After 1 hour, the proximal, middle, and distal segments were taken from the small intestine and the degree of damage was analyzed. In each segment, the expression of HSPs was analyzed by western blotting. The expression of inflammatory mediators including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), and antioxidant enzyme such as glutathione-S-transferase were compared using real-time polymerase chain reaction assays. ResultsIn the control group, HSP70 increased in all segments of small intestine. Additionally, increases in the expression of HSP40 and HSP90 in the distal regions and an increase in HSP32 in the middle regions were observed. After ethanol treatment, greater histological damage was observed in the distal small intestine and significant decreases in HSPs were observed generally. Increased expression of IL-1β, TNF-α, and COX-2 was observed in small intestinal tissues exposed to ethanol-induced damage. However, there was no significant difference in the expression of an antioxidant enzyme. ConclusionsSignificant differences in the expression of HSPs in different intestinal regions were observed. These differences may have been attributable to the distribution of intestinal bacteria.
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Citations
Citations to this article as recorded by  - Ethanol-induced changes to the gut microbiome compromise the intestinal homeostasis: a review
Konrad Sosnowski, Adam Przybyłkowski
Gut Microbes.2024;[Epub] CrossRef - The Influence of Alcohol Consumption on Intestinal Nutrient Absorption: A Comprehensive Review
Molly Butts, Vijaya Lakshmi Sundaram, Usha Murughiyan, Alip Borthakur, Soudamani Singh
Nutrients.2023; 15(7): 1571. CrossRef - Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota
Marie-Edith Arnal, Jean-Paul Lallès
Nutrition Reviews.2016; 74(3): 181. CrossRef - Protéines du choc thermique inductibles dans l’épithélium intestinal : propriétés protectrices et modulation par le microbiote et des facteurs alimentaires
Marie-Édith Arnal, Jean-Paul Lallès
Cahiers de Nutrition et de Diététique.2016; 51(4): 186. CrossRef - Preinduction of heat shock protein 70 protects mice against post-infection irritable bowel syndrome via NF-κB and NOS/NO signaling pathways
Xuchun Zhou, Liwei Dong, Bo Yang, Zhoutao He, Yiyao Chen, Taozhi Deng, Baili Huang, Cheng Lan
Amino Acids.2015; 47(12): 2635. CrossRef
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Effect of Aspirin on Nuclear β-Catenin Expression in Sporadic Colorectal Adenomas
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Hee Jung Kim, Sung Joon Lee, Sung Chul Park, Dae Hee Choi, Chang Don Kang, Gu Kang
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Intest Res 2013;11(4):283-291. Published online October 30, 2013
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DOI: https://doi.org/10.5217/ir.2013.11.4.283
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Abstract
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In addition to the inhibition of cyclooxygenase-2, the chemopreventive effect of non-steroidal anti-inflammatory drugs on the nuclear translocation of β-catenin has been suggested in patients with familial adenoma polyposis. We investigated the effect of aspirin on the β-catenin signaling pathway in patients with sporadic colorectal adenoma. Methods: We selected patients diagnosed with colorectal adenoma. Patients who had been taking aspirin for more than 12 months were identified as the aspirin group, and those who did not were the non-aspirin group. Their characteristics, including size and degree of dysplasia, were compared. Immunohistochemical staining was conducted and the expression levels of nuclear β-catenin and cyclin D1 were investigated. Results: The median duration of aspirin intake was 37 months; there were no significant differences in the size, histological type, and degree of dysplasia between the two groups. Nuclear β-catenin expression was observed in 43.2% of the patients in the aspirin group and in 18.9% of those in the non-aspirin group (P < 0.05). There was no significant difference in nuclear cyclin D1 staining between the aspirin (78.4%) and non-aspirin (91.9%) groups. Conclusions: In this retrospective study, nuclear β-catenin expression in sporadic colorectal adenoma in the aspirin group was not inhibited compared with that in the non-aspirin group. Therefore, further prospective studies with a large number of patients are necessary. (Intest Res 2013;11:283-291)
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Citations
Citations to this article as recorded by - Dose Aspirin Inhibit the Expression of Nuclear β-CateninIn VivoAs It DoesIn VitroStudies?
Dong-Hoon Yang
Intestinal Research.2013; 11(4): 236. CrossRef
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Clinical Significance of Serum C-Reactive Protein in Patients with Colorectal Cancer
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Sung Chul Park, Yoon Tae Jeen, Kwang Gyun Lee, Juhyung Kim, Jong Jin Hyun, Eun Sun Kim, Sanghoon Park, Bora Keum, Yeon Seok Seo, Yong Sik Kim, Hoon Jai Chun, Soon Ho Um, Jai Hyun Choi, Chang Duck Kim, Ho Sang Ryu
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Intest Res 2009;7(2):93-99. Published online December 30, 2009
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Abstract
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C-reactive protein (CRP) is a general marker of inflammation and increased CRP level is reported in several cancers. It has been reported that CRP is an independent factor predicting survival in colorectal cancer patients, although this claim is still under debate. The aim of this study was to investigate the association between CRP and the characteristics of colorectal cancer patients. Methods: One hundred eighty-four patients diagnosed with colorectal cancer between January 2007 and January 2009 were included. The patients with active infectious diseases, other tumors, cardiovascular disease, or inflammatory bowel disease were excluded. The CRP levels of colorectal cancer patients were compared with the control group comprised of 175 healthy adults with a normal colonoscopy. Results: The median CRP in the colorectal cancer patients (3.36 mg/L) was higher than the control group (0.48 mg/L). There was a significant correlation between CRP and the stage of colorectal cancer (p＜0.001). CRP was increased significantly in Dukes' stage D. CRP had a significant correlations with the CEA and CA 19-9 levels, the ESR, and the white blood cell count, and an inverse correlation with albumin. The CRP level in colon cancer patients was higher than rectal cancer patients (p=0.032). There were no significant difference in the CRP according to metastatic sites, such as the liver and peritoneum. Conclusions: Serum CRP levels were higher in patients with colorectal cancer and high CRP level is a predictor of advanced disease. (Intest Res 2009;7:93-99)
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