Cadmium Exacerbates Acetic Acid Induced Experimental Colitis in Rats

Adegoke Ag, A. Salami, S. Olaleye
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引用次数: 5

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.
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镉加重醋酸诱导大鼠实验性结肠炎
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。
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