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作 者:徐建虎[1,2] 张琦[1] 杨子庆[1] 罗炽琼 李雷兵[1] 任小彤 李林鲜[1] 徐路[1] 肖桦[1]
机构地区:[1]成都中医药大学,四川610075 [2]宁夏医科大学中医学院
出 处:《北京中医药大学学报》2015年第11期749-752,共4页Journal of Beijing University of Traditional Chinese Medicine
基 金:国家自然科学基金资助项目(No.81273644)
摘 要:目的探讨温阳消饮法消除水饮的部分作用机制。方法 Wistar大鼠随机分为空白组和A组,A组动物采用阿霉素(Adr)腹腔注射制备慢性心力衰竭(CHF)模型。造模结束后将A组大鼠再随机分为:模型组、温阳消饮组、去桂消饮组。1温阳消饮组:按12 g/(kg·d)等效剂量灌胃给予温阳消饮方药液,每日1次,连续4周;2去桂消饮组:按10 g/(kg·d)等效剂量灌胃给予去桂消饮方药液,每日1次,连续4周;3模型组、空白组:同等条件饲养,不实施任何给药方案。结果与空白组相比,模型组血清脑钠素(BNP)含量明显升高,肾脏组织中水通道蛋白2(AQP2)蛋白表达降低,差异有显著性(P<0.05或P<0.01);与模型组相比,温阳消饮组、去桂消饮组血清BNP含量明显降低,肾脏中AQP2蛋白表达增加,差异有显著性(P<0.05或P<0.01)。结论温阳消饮法可显著降低CHF模型大鼠血清BNP含量,上调CHF模型大鼠肾组织AQP2的表达。Objective To explore the potential mechanism of eliminating fluid-retention by yang-warming and fluid retention-resolving method. Methods Rat model of congestive heart failure( CHF) was established by intraperitoneal injection of adriamycin. After modeling,the CHF rats were randomly divided into model group,group of yang-warming and fluid retention-resolving formula( YWFRR group),and group of yang-warming and fluid retention-resolving formula minus cinnamon twig( YWFRR-CT group).The rats of YWFRR group were intragastrically administered( i. g.) YWFRR at the dose of 12 g / kg once daily for consecutive four weeks,and those of YWFRR-CT were i. g. YWFRR-CT at the dose of 10 g / kg once daily for four weeks,at the same time,the rats of model group and blank group took no medication treatment. Then the serum level of brain natriuretic peptide( BNP) and protein expression of aquaporin-2( AQP2) in renal tissue were determined. Results Compared with the blank group,the serum content of BNP in model group increased significantly and the expression of AQP2 in renal tissue decreased significantly( P 0. 05 or P 0. 01). The contents of serum BNP were both lower in YWFRR group and YWFRR-CT group than that of model group,and the expression of AQP2 higher. Conclusion The method of yang-warming and fluid retention-resolving could decrease the serum content of BNP and upregulate the expression of renal AQP2 of CHF rats.
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