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作 者:王军[1] 叶章群[2] 宋波[1] 金锡御[1] 杨为民[2] 王少刚[2] 周四维[2]
机构地区:[1]第三军医大学西南医院全军泌尿外科中心,重庆400038 [2]华中科技大学同济医学院附属同济医院泌尿外科,武汉430030
出 处:《第三军医大学学报》2005年第23期2341-2344,共4页Journal of Third Military Medical University
摘 要:目的了解前列腺素E2在尿结石形成中的作用以及α-亚麻酸对草酸钙结石鼠前列腺素E2、肾草酸钙结晶形成的抑制作用。方法60只雄性Wistar成年大鼠随机分成4组,分别喂饲苏子油、葵花籽油4周后,使用诱石剂1%乙二醇(EG)加1%氯化氨喂饮大鼠,同时继续以苏子油和葵花籽油灌胃,3周后检测各组大鼠肾功能,24h血尿生化指标,肾草酸钙结晶情况及各组大鼠尿前列腺素E2水平。结果苏子油组肾组织水肿较轻,肾内草酸钙结晶数及肾钙含量明显低于成石组(P<0·01),24h尿钙排泄,血尿素氮,肌酐浓度显著低于成石组(P<0·05),尿肌酐排泄增加(P<0·05)。葵花籽油组仅血尿肌酐较成石组明显改善(P<0·05),其他指标与成石组无显著差异(P>0·05)。24h尿前腺素E2水平苏子油组、对照组显著低于成石组(P<0·01、P<0·05)。葵花籽油组与成石组比较无显著性差异(P>0·05)。成石组、苏子油组、葵花籽油组前列腺素E2水平与尿总钙含量成正相关性。结论前列腺素E2可能参与并促进了尿结石的形成,α-亚麻酸可能通过抑制肾前列腺素E2的产生而抑制尿结石形成。inhibitory effect rats. Methods Objective To investigate the role of of α-linolenic acid on renal prostaglan renal prostaglandin E2 in urinary stone formation and the dins and renal calcium oxalate crystallization in urolithic A total of 60 male adult rats were randomly assigned into 4 groups. The rats were administered with tap water for 4 weeks, then 3 groups were induced to lithogenesis by administration of 1% ethanediol and 1% ammonia chloride for 3 weeks accompanied with everyday intragastric administration of tap water (group B), or 2 g Perilla frutescens ( L · ) Britt · oil ( group C), or 2 g sunflower seeds oil ( group D). All rats were sacrificed and the renal tissue calcium, the urinary calcium, the calcium oxalate crystallization, urinary oxalate and urinary prostaglandin E2 were detected. Results The hydronephrosis and parenchymal swelling in group C were obviously slight as compared with that of group B, and the calcium oxalate crystalization, renal tissue calcium, urinary calcium excretion, blood urea nitrogen and creatinine of group C were also significantly lower than those of group B ( P 〈 0. 05 ). The oxalate excretion and magnesium/calcium ratio in group D were of no significance with that of group B, but the blood and urinary creatinine were lower in group D (P 〈 0. 05 ). The 24-hour urinary PGE2 in groups C and A was significantly lower than group B ( P 〈 0. 01, P 〈 0. 05 ), but no significant difference between groups B and D. There was a significant correlation among groups B, C, D in PGE2 and urinary calcium. Conclusion This study suggests that the renal prostaglandin E2 may participate in calcium stone formation, and α-linolenic acid may prevent calcium oxalate lithogenesis by inhibiting the renal prostaglandin E2.
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