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1. 南方医科大学南方医院消化科,广东,广州,510515
2. 韶关市铁路医院消化科,广东,韶关,512023
Published Online:07 March 2014,
Published:07 March 2014
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袁葵,郭文,朱明古. 芥菜籽通过抗氧化和免疫偏移预防大肠肿瘤的实验研究[J]. 中国癌症杂志, 2014, 24(2): 93-98.
袁葵, 郭文, 朱明古. Experimental study of mustard seeds prevent colorectal tumor by antioxidation and immune deviation[J]. China Oncology, 2014, 24(2): 93-98.
袁葵,郭文,朱明古. 芥菜籽通过抗氧化和免疫偏移预防大肠肿瘤的实验研究[J]. 中国癌症杂志, 2014, 24(2): 93-98. DOI: 10.3969/j.issn.1007-3969.2014.02.003.
袁葵, 郭文, 朱明古. Experimental study of mustard seeds prevent colorectal tumor by antioxidation and immune deviation[J]. China Oncology, 2014, 24(2): 93-98. DOI: 10.3969/j.issn.1007-3969.2014.02.003.
背景与目的:近年来有关十字花科植物预防肿瘤的研究,主要探讨其抗氧化、抗突变作用、调节免疫功能及诱导细胞凋亡等。芥菜籽(mustard seeds,MS)是十字花科植物的种子。本研究旨在探讨MS对1
2-二甲基肼(1
2-dimethylhydrazine,DMH)诱导的大鼠大肠肿瘤的抗氧化和免疫偏移作用机制。方法:将48只Wistar雄性大鼠随机均分为4组:DMH模型组(模型组)、DMH+5%MS干预组(5%MS干预组)、DMH+7.5%MS干预组(7.5%MS干预组)和正常对照组。模型组和MS干预组每周按30 mg/kg剂量给予DMH腹腔注射1次,连续20周,均于32周时处死大鼠观察大肠肿瘤发生率并HE染色确定肿瘤的组织分型,检测血清脂质过氧化产物丙二醛(malondialdehyde,MDA)水平、抗氧化酶活力、Th1和Th2亚群细胞因子含量。结果:正常对照组大鼠无肿瘤发生。模型组总成瘤率为100%,5%MS干预组和7.5%MS干预组总成瘤率分别降低33.3%和58.3%(P0.05)。DMH诱导大鼠形成肿瘤的过程中,模型组MDA水平和Th2亚群细胞因子含量均显著高于正常对照组(P0.05);而抗氧化酶活力明显低于正常对照组(P0.05)。经MS干预后MDA呈显著下降趋势(P0.05),而抗氧化酶活力和Th1亚群细胞因子含量均呈显著升高趋势(P0.05)。结论:芥菜籽显著降低DMH化学诱导的大鼠大肠肿瘤的发生,作用机制可能与其抗氧化作用和免疫平衡偏移有关。
Background and purpose: Recently
a large number of researches have shown that cruciferous plants have the chemopreventive effect on tumor. Mechanisms of antitumorigenesis were investigated on antioxidation
antimutation
immunity and inducing apoptosis
and so on. Mustard seeds (MS) are the seeds belong to the cruciferous plants. This study aimed to investigate antioxidation and immune deviation of MS on colorectal tumor in rats induced by 1
2-dimethylhydrazine (DMH). Methods: A total of 48 male Wistar rats were randomly divided into four groups: DMH alone
DMH+5%MS
DMH+7.5%MS
and the untreated control group(Saline). Colorectal tumorigenesis was induced by intraperitoneal injecting 30 mg/kg DMH once a week for 20 weeks. At the end of 32 weeks
the rats were sacrificed
then colorectal tumor incidence was observed and histological type was determined by HE staining. A colorimetric assay was used to detect levels of the lipid peroxidation product malondialdehyde (MDA) and the activity of antioxidant enzymes in the serum of all rats. The levels of Th1 and Th2 cytokines were detected with Luminex200. Results: No tumorous lesion was found in the untreated control group. However
the total tumor incidence in DMH+5%MS group and DMH+7.5%MS group was significantly decreased 33.3% and 58.3% respectively
compared with the DMH group’s (100%
P0.05). As DMH induced colorectal tumorigenesis
MDA and Th2 cytokines in the serum were significantly higher in the DMH group than those in the untreated control group (P0.05)
but the activities of antioxidant enzymes were significantly lower (P0.05). While the MS treatment
compared with the DMH group
significantly suppressed the MDA level but enhanced the activities of antioxidant enzymes and levels of Th1 cytokines (P0.05). Conclusion: MS significantly decrease prevalence rates of DMH-induced colorectal tumor in rats. The mechanism may be related with the antioxidation and immune balance deviation.
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