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海兔素对酒精性肝损伤大鼠NF-кB、iNOS及COX-2的影响

发布时间:2018-03-14 06:11

  本文选题:海兔素 切入点:酒精性肝损伤 出处:《卫生研究》2015年02期  论文类型:期刊论文


【摘要】:目的通过观察酒精性肝损伤大鼠NF-кB p65、i NOS和COX-2的表达,探讨海兔素对酒精性肝损伤的保护机制。方法 (1)8周龄雄性Wistar大鼠,按体重随机分为6组(空白对照组,酒精模型组,阳性对照组,海兔素低、中、高剂量组),每组10只。各组均采用灌胃方式给药,每日一次,连续6周。除空白对照组每日灌胃生理盐水外,其余各组前2周每日给予50%乙醇8 ml/kg,后4周提高至12 ml/kg。海兔素低、中、高剂量组每日还同时分别给予海兔素50、100和150 mg/kg BW,阳性对照组则每日给予200 mg/kg甘草酸二铵。实验结束后ELISA法检测大鼠血浆中i NOS和COX-2活性。(2)8周龄成年雄性Wistar大鼠45只,按体重随机分为3组,空白对照组每日生理盐水灌胃,酒精模型组和海兔素组每日给予50%乙醇8 ml/kg灌胃2周,然后将剂量提高至12 ml/kg,持续6周。海兔素组每日酒精灌胃前4 h,先给予150 mg/kg海兔素灌胃。8周后经二步胶原酶技术分离培养获取大鼠原代肝细胞,每组大鼠各获得一组原代肝细胞。Western Blot法检测大鼠原代肝细胞NF-кB p65蛋白的表达。结果酒精模型组i NOS与COX-2活性均明显高于空白对照组(P0.05);与酒精模型组相比,海兔素低、中、高剂量组i NOS、COX-2活性均有所降低(P0.05)。并且海兔素高剂量组i NOS及COX-2的活性与阳性对照组相比差异无统计学意义。酒精模型组NF-кB p65蛋白的表达明显高于空白对照组(P0.05),是空白对照组的1.5倍;而海兔素干预组NF-кB p65蛋白表达明显被抑制(P0.05),与酒精模型组相比,下降52.7%。结论海兔素可通过抑制NF-кB、i NOS及COX-2的表达,对酒精性肝损伤起到一定的保护作用。
[Abstract]:Objective to observe the expression of NOS and COX-2 in rats with alcoholic liver injury and to explore the protective mechanism of haitulin on alcoholic liver injury. Methods male Wistar rats of 8 weeks old were randomly divided into 6 groups according to their body weight (blank control group, alcohol model group). Positive control group, low, medium and high dose groups, 10 rats in each group. Each group was administered by gavage once a day for 6 weeks, except for the blank control group. The other groups were given 50% ethanol 8 ml / kg per day for the first 2 weeks and increased to 12 ml / kg for 4 weeks. The high dose group was also given 50,100 and 150 mg/kg BW daily, while the positive control group was given 200 mg/kg diammonium glycyrrhizinate daily. After the experiment, the plasma I NOS and COX-2 activities were detected by ELISA method in 45 adult male Wistar rats at the age of 8 weeks. The rats were randomly divided into 3 groups according to their body weight. The blank control group was fed with normal saline daily, the alcohol model group and the sea rabbit group were given 50% ethanol 8 ml/kg daily for 2 weeks. Then the dose was increased to 12 ml / kg for 6 weeks. The primary rat hepatocytes were isolated and cultured by two-step collagenase technique 4 hours before alcohol was given to the rats in the sea rabbit injection group for 4 hours before oral administration for 1. 8 weeks, and then cultured by two steps collagenase technique, and the primary rat hepatocytes were isolated and cultured by two steps collagenase technique. One group of primary hepatocytes was obtained from each group. Western Blot assay was used to detect the expression of NF- NOS B p65 protein in primary rat hepatocytes. Results the activities of I NOS and COX-2 in the alcohol model group were significantly higher than those in the control group (P 0.05). The activity of COX-2 was decreased in high dose group, and the activity of I NOS and COX-2 in high dose group was not significantly different from that in positive control group. The expression of NF- FB p65 protein in alcohol model group was significantly higher than that in control group (P 0. 05), and the expression of I NOS and COX-2 in high dose group was significantly higher than that in control group (P 0. 05). 1.5 times of the blank control group; However, the expression of NF-1 B p65 protein was significantly inhibited in the sea rabbit intervention group, which was 52.7% lower than that in the alcohol model group. Conclusion it can protect the alcoholic liver injury by inhibiting the expression of NOS and COX-2.
【作者单位】: 青岛大学医学院营养研究所;青岛大学医学院细胞与分子生物学实验室;
【基金】:国家自然科学基金(No.31171671) “十二五”农村领域国家科技计划课题(No.2012BAD33B01-2)
【分类号】:R151

【参考文献】

相关期刊论文 前6条

1 赵彩彦;核因子-κB与酒精性肝病[J];国外医学(消化系疾病分册);2002年04期

2 刘禹;兰海楠;李维;杨艳红;付志玲;马思慧;吴天成;郭风;赵雪;张辉;崔焕忠;吴e,

本文编号:1609962


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