摘要
目的探讨维生素D在2.5%硫酸葡聚糖钠(DSS)诱导的实验性肠炎中的作用。方法随机抽取C57BL/6源性的野生小鼠10只和VDR敲除小鼠10只分别为对照组和实验组,将DSS加入饮用水中配成2.5%DSS溶液分别喂食,评估两组症状评分及生存时间。另行体外实验,应用5%的DSS溶液刺激Caco-2细胞单层,实验组加入1,25(OH)2D3,对照组不予额外处理,测量两组细胞跨膜电阻。结果正常野生鼠对2.5%DSS诱导的实验性肠炎可耐受,VDR敲除鼠出现严重腹泻,直肠出血,体重显著降低等,相对于对照组症状评分增高,生存时间缩短。对照组的细胞跨膜电阻在4 h内逐渐下降,而实验组细胞的跨膜电位在初始阶段有所下降,4 h后恢复正常。结论维生素D在2.5%DSS诱导的实验性肠炎中能够起到保护作用。在体外试验中,1,25(OH)2D3能够抵御DSS诱导的实验性肠炎,为进一步研究维生素D及其信号系统的功能提供了理论依据。
Objective To explore the effect of vitamin D on 2. 5% DSS-induced experimental colitis. Methods Wild and vitamin D receptor( VDR) knockout C57 BL /6 mice were divided into control group( n = 10,wild)and experimental group( n = 10,VDR knockout). The mice were fed with 2. 5% DSS. The symptom score and life time was observed. In vitro experiments: when Caco-2 monolayers were stimulated with 5% DSS,experimental group was added with 1,25( OH)2D3. The TEER of both groups was determined. Results The mice in control group were mostly resistant to 2. 5% DSS-induced experimental colitis. There were a lot of symptoms such as severe diarrhea,rectal bleeding and marked body weight loss in the mice of experimental group. The symptom score of experimental group was higher than that of control group with shorter life time. The TEER gradually decreased within 4 h in control group,in experimental group,the TEER was moderately reduced at the beginning and fully recovered after 4 h. Conclusion Vitamin D can play a protective role on 2. 5% DSS-induced experimental colitis,which provides a theoretical evidence for further study of vitamin D and the function of its signal system.
出处
《实用药物与临床》
CAS
2015年第6期635-638,共4页
Practical Pharmacy and Clinical Remedies
基金
国家自然科学基金(30971401
81170065)
辽宁省攀登学者计划
辽宁省十百千计划