文献类型：期刊文献

中文题名：贝那普利和氨氯地平对自发性高血压大鼠十二指肠、脑组织胆囊收缩素表达的影响

英文题名：The influences of benazepril and amlodipine on the expressions of cholecystokinin in the duodenum and brain of spontaneously hypertensive rats

作者：金华[1,2];刘志军[1];颜春鲁[1];刘峰林[1];陈丽[1];张秋菊[1];徐厚谦[1];胡继宏[1];窦荣海[1];温鑫洋[1];曹强[1];苏莉莉[1]

第一作者：金华

机构：[1]甘肃中医药大学;[2]甘肃省中医方药挖掘与创新转化重点实验室

第一机构：甘肃中医药大学

年份：2017

卷号：25

期号：6

起止页码：548

中文期刊名：中华高血压杂志

外文期刊名：Chinese Journal of Hypertension

收录：CSTPCD;;北大核心:【北大核心2014】；CSCD:【CSCD2017_2018】；

基金：国家自然科学基金资助项目(81160477);甘肃省自然科学研究基金计划(1107RJZA220);甘肃省高等学校基本科研业务费资助项目(2010-5)

语种：中文

中文关键词：自发性高血压大鼠;胆囊收缩素;贝那普利;氨氯地平

外文关键词：spontaneously hypertensive rats ; cholecystokinin; benazepril; amlodipine

摘要：目的探讨贝那普利和氨氯地平对自发性高血压大鼠(SHR)胆囊收缩素(CCK)mRNA及蛋白表达的影响。方法 45只14周龄雄性SHR随机分为SHR组(n=15)、贝那普利组[盐酸贝那普利灌服0.90mg/(kg·d),n=15]、氨氯地平组[苯磺酸氨氯地平灌服0.45mg/(kg·d),n=15],另以Wistar-Kyoto(WKY)大鼠作为正常对照组(n=15),SHR组及WKY组每日灌服同体积的蒸馏水,干预8周,测定各组大鼠安静清醒状态下尾动脉压,应用酶联免疫吸附试验(ELISA)法检测血清中CCK的含量;采用逆转录聚合酶链反应(RT-PCR)检测十二指肠中CCK mRNA表达;采用Western blot法检测十二指肠和脑中CCK蛋白表达。结果干预8周后,与WKY组比较,SHR组血压升高[收缩压/舒张压(201.0±14.6)/(157.4±16.2)比(136.3±12.0)/(102.9±10.2)mm Hg],十二指肠中CCK mRNA和蛋白表达显著降低,脑中CCK蛋白表达显著降低(均P<0.05),但血清CCK水平差异无统计学意义(P>0.05);与SHR组比较,贝那普利组与氨氯地平组血压降低[(181.5±17.5)/(145.4±18.3)、(188.4±14.5)/(145.6±13.8)比(201.0±14.6)/(157.4±16.2)mm Hg,均P<0.05],贝那普利组与氨氯地平组十二指肠中CCK mRNA和蛋白表达、脑中CCK蛋白表达显著升高(均P<0.05)。结论 SHR十二指肠和脑组织中CCK调节失衡,贝那普利和氨氯地平可能通过调节CCK的表达而降压。
Objective To investigate the influences of benazepril and amlodipine on the expressions of mRNA and protein of cholecystokinin （CCK） in spontaneously hypertensive rats （SHR）. Methods Forty-five SHR （14 weeks old, male） were randomly assigned into SHR group （n=15） , benazepril group [SHR were given 0.90 mg/（kg · d） dose of benazepril by gavage, n=15] and amlodipine group [SHR were given 0.45 mg/（kg · d） dose of amlodipine by gavage, n= 15]. Wistar-Kyoto （WKY） rats were taken as the normal control group （n= 15）, and the rats in the SHR group and WKY group were given the same volume of distilled water once a day by gavage. After the in- tervention for 8 weeks, the tail arterial pressure of all rats was measured in the quiet and sober state. The level of serum CCK was detected by enzyme linked immunosorbent assay（ELISA）, and the expression of CCK mRNA in the duodenum was detected by reverse transcription polymerase chain reaction（RT-PCR）, and the expressions of CCK protein in the duodenum and brain were detected by Western blot. Results After the intervention for 8 weeks, compared with the WKY group, the blood pressure was significantly increased [systolic/diastolic blood pressure （201.0±14.6）/（157.4±16.2） vs （136.3±12.0）/（102.9±10.2） mmHg], while the expressions of CCK mRNA and protein in the duodenum and the expression of CCK protein in the brain were significantly decreased in the SHR group （all P〈0.05）. While there were no differences in the level of serum CCK between the two groups （P〉 0.05）. Compared with the SHR group, the blood pressure was significantly decreased [systolic/diastolic blood pressure （181.5±17.5）/{145.4±18.3）, （188.4±14.5）/（145.6±13.8） vs （201.0±14.6）/（157.4±16.2）mmHg, all P〈0. 05], while the expressions of CCK mRNA and protein in the duodenum and the expression oI CCK protein in the brain were significantly increased in the benazepril group and amlodipine group （all P〈 0.05 ）. Conclusion The regulation disorder of CCK existed in the duodenum and brain tissue of SHR. Benazepril and amlodipine could lower blood pressure possibly by regulating the expression of CCK.