镉加重醋酸诱导大鼠实验性结肠炎

Adegoke Ag, A. Salami, S. Olaleye
{"title":"镉加重醋酸诱导大鼠实验性结肠炎","authors":"Adegoke Ag, A. Salami, S. Olaleye","doi":"10.21767/2248-9215.100027","DOIUrl":null,"url":null,"abstract":"Background: Increase in the incidences of inflammatory bowel disease (IBD) in developing countries is a pointer to the role metal toxicants may play in its pathogenesis. Cadmium (Cd) has been implicated in the etiology of diseases involving several tissues including the colonic mucosa. This present study aimed at investigating the effects of oral cadmium exposures on healing of acetic acid (AA)-induced colitis in rats. Methods and Findings: Male Wistar rats (100-120 g) were grouped and exposed to cadmium as follows: Control (water), Cd25 (25 ppm CdCl2), Cd50 (50 ppm CdCl2), Cd100 (100 ppm CdCl2) for four weeks. Colitis was induced by intrarectal administration of 2 ml 4% acetic acid. Rats were sacrificed and colons were resected on days 0, 3, 7 and 14 of colitis induction. Weekly body weight, diarrheal and macroscopic scores, organ weights, neutrophil/lymphocyte ratio (NLR), malondialdehyde (MDA) concentration, and regeneration in colonic tissues were studied microscopically. Cadmium significantly (p<0.05) decreased weight gain (%) at weeks 3 and 4 in Cd100 group, significantly (p<0.05) increased stool consistency scores on day 5 in Cd100 group, increased colon macroscopic scores in Cd100 group on days 3 and 7, significantly (p<0.05) increased neutrophil/ lymphocyte ratio on days 0 and 7 in Cd50 and Cd100, and colonic MDA concentrations in each of Cd25, Cd50 and Cd100 from day 3 till day 14. Colon histopathology persisted till day 14 in Cd100 group. Conclusions: These data indicate that cadmium delayed healing of acetic acid induced colitis and inflammatory pathways may be implicated.","PeriodicalId":12012,"journal":{"name":"European Journal of Experimental Biology","volume":"8 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"5","resultStr":"{\"title\":\"Cadmium Exacerbates Acetic Acid Induced Experimental Colitis in Rats\",\"authors\":\"Adegoke Ag, A. Salami, S. Olaleye\",\"doi\":\"10.21767/2248-9215.100027\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background: Increase in the incidences of inflammatory bowel disease (IBD) in developing countries is a pointer to the role metal toxicants may play in its pathogenesis. Cadmium (Cd) has been implicated in the etiology of diseases involving several tissues including the colonic mucosa. This present study aimed at investigating the effects of oral cadmium exposures on healing of acetic acid (AA)-induced colitis in rats. Methods and Findings: Male Wistar rats (100-120 g) were grouped and exposed to cadmium as follows: Control (water), Cd25 (25 ppm CdCl2), Cd50 (50 ppm CdCl2), Cd100 (100 ppm CdCl2) for four weeks. Colitis was induced by intrarectal administration of 2 ml 4% acetic acid. Rats were sacrificed and colons were resected on days 0, 3, 7 and 14 of colitis induction. Weekly body weight, diarrheal and macroscopic scores, organ weights, neutrophil/lymphocyte ratio (NLR), malondialdehyde (MDA) concentration, and regeneration in colonic tissues were studied microscopically. Cadmium significantly (p<0.05) decreased weight gain (%) at weeks 3 and 4 in Cd100 group, significantly (p<0.05) increased stool consistency scores on day 5 in Cd100 group, increased colon macroscopic scores in Cd100 group on days 3 and 7, significantly (p<0.05) increased neutrophil/ lymphocyte ratio on days 0 and 7 in Cd50 and Cd100, and colonic MDA concentrations in each of Cd25, Cd50 and Cd100 from day 3 till day 14. Colon histopathology persisted till day 14 in Cd100 group. Conclusions: These data indicate that cadmium delayed healing of acetic acid induced colitis and inflammatory pathways may be implicated.\",\"PeriodicalId\":12012,\"journal\":{\"name\":\"European Journal of Experimental Biology\",\"volume\":\"8 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2017-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"5\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European Journal of Experimental Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.21767/2248-9215.100027\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Experimental Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21767/2248-9215.100027","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5

摘要

背景:发展中国家炎症性肠病(IBD)发病率的增加表明金属毒物可能在其发病机制中发挥作用。镉(Cd)与包括结肠粘膜在内的多种组织的疾病的病因学有关。本研究旨在探讨口服镉暴露对大鼠醋酸(AA)诱导结肠炎愈合的影响。方法与发现:雄性Wistar大鼠(100-120 g)按以下方式暴露于镉:对照(水)、Cd25 (25 ppm CdCl2)、Cd50 (50 ppm CdCl2)、Cd100 (100 ppm CdCl2) 4周。用2 ml 4%醋酸直肠内灌胃诱导结肠炎。在结肠炎诱导的第0、3、7、14天处死大鼠,切除结肠。显微镜下观察各组大鼠每周体重、腹泻和宏观评分、器官重量、中性粒细胞/淋巴细胞比(NLR)、丙二醛(MDA)浓度和结肠组织再生情况。镉显著(p<0.05)降低了Cd100组小鼠第3、4周的增重(%),显著(p<0.05)提高了Cd100组小鼠第5天的粪便一致性评分,显著(p<0.05)提高了Cd100组小鼠第3、7天的结肠宏观评分,显著(p<0.05)提高了Cd50和Cd100小鼠第0、7天的中性粒细胞/淋巴细胞比值,以及第3 ~ 14天Cd25、Cd50和Cd100小鼠结肠MDA浓度。Cd100组结肠组织病理学持续到第14天。结论:这些数据表明,镉延迟醋酸诱导结肠炎的愈合和炎症途径可能涉及。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Cadmium Exacerbates Acetic Acid Induced Experimental Colitis in Rats
Background: Increase in the incidences of inflammatory bowel disease (IBD) in developing countries is a pointer to the role metal toxicants may play in its pathogenesis. Cadmium (Cd) has been implicated in the etiology of diseases involving several tissues including the colonic mucosa. This present study aimed at investigating the effects of oral cadmium exposures on healing of acetic acid (AA)-induced colitis in rats. Methods and Findings: Male Wistar rats (100-120 g) were grouped and exposed to cadmium as follows: Control (water), Cd25 (25 ppm CdCl2), Cd50 (50 ppm CdCl2), Cd100 (100 ppm CdCl2) for four weeks. Colitis was induced by intrarectal administration of 2 ml 4% acetic acid. Rats were sacrificed and colons were resected on days 0, 3, 7 and 14 of colitis induction. Weekly body weight, diarrheal and macroscopic scores, organ weights, neutrophil/lymphocyte ratio (NLR), malondialdehyde (MDA) concentration, and regeneration in colonic tissues were studied microscopically. Cadmium significantly (p<0.05) decreased weight gain (%) at weeks 3 and 4 in Cd100 group, significantly (p<0.05) increased stool consistency scores on day 5 in Cd100 group, increased colon macroscopic scores in Cd100 group on days 3 and 7, significantly (p<0.05) increased neutrophil/ lymphocyte ratio on days 0 and 7 in Cd50 and Cd100, and colonic MDA concentrations in each of Cd25, Cd50 and Cd100 from day 3 till day 14. Colon histopathology persisted till day 14 in Cd100 group. Conclusions: These data indicate that cadmium delayed healing of acetic acid induced colitis and inflammatory pathways may be implicated.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Histochemical Effects of Aloe Vera Gel (Aloe Barbadensis Miller) on Puncture-Induced Intervertebral Disc Degeneration in Rabbits Tetralogy of Fallot: Origins, Management and Outcomes Profiling the Nitrogen Efficiency Using Agricultural Engineering Technique of YARA ALS Tractor Senso Pollen Variations among some Cultivated Citrus Species and its Related Genera in Egypt Bruton’s Tyrosine Kinase (Btk) Inhibitor Tirabrutinib Prevents the Development of Murine Lupus
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1