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作 者:孙晓霞 战丽彬[1] 侯圣林 江玉翠 杨关林[2] Sun Xiaoxia;Zhan Libin;Hou Shenglin;Jiang Yucui;Yang Guanlin(Basic Medical College,Modern Research Laboratory of Spleen Visceral Manifestations Theory,Nanjing University of Chinese Medicine,Nanjing 210023,China;Liaoning University of Traditional Chinese Medicine,Shenyang 110032,China)
机构地区:[1]南京中医药大学基础医学院,中医脾藏象现代研究实验室,南京210023 [2]辽宁中医药大学,沈阳110032
出 处:《世界科学技术-中医药现代化》2018年第5期660-665,共6页Modernization of Traditional Chinese Medicine and Materia Medica-World Science and Technology
基 金:国家科学技术部国家重点基础研究发展计划(973计划)项目(2013CB531704):"脾虚生痰"所致冠心病心绞痛"从脾论治"疗效机制及规律研究;负责人:杨关林;江苏省人民政府江苏高校优势学科建设工程资助项目:中医学科建设;负责人:方祝元;江苏省教育厅江苏省研究生科研与实践创新计划(KYCX18_1534):脾阴虚大鼠肠黏膜屏障变化及滋补脾阴方药干预作用研究;负责人:孙晓霞
摘 要:目的:观察脾阴虚大鼠空肠葡萄糖转运蛋白1(GLUT1)、葡萄糖转运蛋白5(GLUT5)m RNA与蛋白表达的变化,以及滋补脾阴方药(ZBPYR)的干预作用。方法:利用饮食失常兼过劳结合燥热耗伤阴液法进行脾阴虚大鼠模型的复制,将SPF级雄性Wistar大鼠随机分为正常组、脾阴虚组和滋补脾阴方药组。使用实时荧光定量PCR(q PCR)法测定空肠GLUT1、GLUT5的m RNA表达,蛋白质印迹(Western Blot)法测定空肠GLUT1、GLUT5的蛋白表达。结果:与正常组比较,脾阴虚组GLUT1、GLUT5的m RNA和蛋白表达量均下降(P<0.05);与脾阴虚组比较,滋补脾阴方药组能够明显上调GLUT1、GLUT5的m RNA表达水平(P<0.01),并增加GLUT1、GLUT5蛋白的表达含量(P<0.05)。结论:通过上调脾阴虚大鼠空肠GLUT1、GLUT5 m RNA和蛋白的表达,可能是ZBPYR对脾阴虚证发挥干预作用的机制之一。Objective: To observe m RNA and protein expressions of jejunal glucose transporter1(GLUT1) and glucose transporter 5(GLUT5) in spleen-yin deficiency(SYD) model rat, as well as the effects of Zibu Piyin Recipe(ZBPYR).Methods: SYD rats were modeled by the method of combination of improper diet, overstrain and injured-yin herbs. The SPF-level male Wistar rats were randomly divided into normal group, SYD group and ZBPYR group. The methods of q PCR and Western Blot were used to determine expressions of GLUT1 and GLUT5. Results: Compared with the normal group, the results showed that expressions of GLUT1, GLUT5 m RNA and protein in SYD group were decreased significantly(P〈0.05). Compared with SYD group, m RNA expressions of GLUT1 and GLUT5 were up-regulated significantly(P〈0.01), and protein expressions of GLUT1 and GLUT5 were also increased(P〈0.05). Conclusion: It was concluded that ZBPYR up-regulated expressions of GLUT1, GLUT5 m RNA and protein in the jejunum of spleen-yin deficiency rats, which may be one of the mechanisms of ZBPYR intervention on spleen-yin deficiency syndrome.
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