摘要
目的 研究芍药苷（Pae）对慢性心力衰竭（CHF）大鼠心肌纤维化的疗效和作用机制。 方法[介绍总共多少只大鼠及分组情况，英摘同改][已修改] 将Wistar大鼠32只随机分为四个组，每组8只大鼠：对照组（Veh组）、模型组（Iso组）、Pae组和卡托普利组（Cap组）。采用异丙肾上腺素（Iso）诱导CHF大鼠心肌纤维化模型，给予Pae （20μg·kg^-1·d^-1）和Cap （15mg·kg^-1·d^-1）连续灌胃6周，利用心脏彩超测量大鼠心脏结构和功能；计算心肌胶原容积分数（CVF）和血管周围胶原面积（PVCA），评价CHF大鼠心肌纤维化程度；行Western Blot和实时荧光PCR检测大鼠心肌组织PTEN mRNA和蛋白表达水平。 结果[结果中请列示主要 数据，英文摘要同改][已修改] 与Iso组相比，Pae和Cap可降低CHF大鼠CVF （13.75 ± 3.77% vs. 30.97 ± 4.22%, P〈0.001；11.90 ± 3.01% vs. 30.97 ± 4.22%, P〈0.001）和PVCA （14.32 ± 2.50% vs. 28.31 ± 3.16%, P〈0.001；15.27 ± 1.24% vs. 28.31 ± 3.16%, P〈0.001），减轻大鼠心肌纤维化程度；Pae和Cap组PTEN mRNA （0.39 ± 0.02 vs. 0.22 ± 0.06, P=0.005；0.50 ± 0.06 vs. 0.22 ± 0.06, P〈0.001）及蛋白（0.49 ± 0.03 vs. 0.11 ± 0.05, P=0.016；0.73 ± 0.22 vs. 0.11 ± 0.05, P=0.007）表达水平较Iso组明显升高。结论 Pae可改善Iso诱导的CHF大鼠心室重构，其作用机制可能与上调PTEN信号通路有关。
[Abstract] Objective To study the effects and mechanism of Paeonifiorin（Pae） on myocardial fibrosis in chronic heart failure （CHF） rats. Methods Thirty-two Wistar rats were randomly divided into 4 groups： vehicle control group （Veh）, isoprenaline model group （Iso）, Pae group and Captopril group （Cap）. There were eight rats in each group. CHF rat model was induced by Iso. Pae （ 20 μg·kg^-1·d^-1 ） and Cap （ 15 mg·kg^-1·d^-1 ） were adminis- trated to CHF rats for six weeks. Cardiac ultrasound was used to assess the structure and function of CHF rats. Col- lagen volume fraction （ CVF ） and per±vascular collagen volume area （PVCA） of myocardial tissues were calculat- ed. With real-time polymerase chain reaction and Western Blot, the protein and mRNA levels of phosphatase and tensin homologue deleted on chromosome ten （PTEN） were detected. Results Compared to Iso group, the levels of CVF[ （ 13.75±3.77）% vs. （30.97±4.22）%, P〈0.001 ; （ 11.90±3.01 ）% vs. （30.97±4.22）%, P〈0.001] and PVCA [ （ 14.32±2.50）% vs. （28.31±3.16）%, P〈0.001 ; （ 15.27±1.24）% vs. （28.31±3.16）%, P〈0.001 ± reduced in Pae and Cap group. Pae and Cap can alleviate the myocardial fibrosis in CHF rats. The expression of PTEN mRNA （0.39±0.02 vs. 0.22±0.06, P=0.005 ; 0.50±0.06 vs. 0.22±0.06, P〈0.001 ） and protein（0.49±0.03 vs. 0.11± 0.05, P：0.016;0.73±0.22 vs. 0.11±0.05, P=0.007） increased markedly in the Pae and Cap treated group. Conclu- sion Pae can attenuate cardiac remodeling in Iso-induced CHF rats. The potential mechanism may be highly asso- ciated with the up-regulating of PTEN signaling pathway.
作者
刘茂
尹枫
陈玲
郑健康
陈剑
LIU Mao;YIN Feng;CHEN Ling(Department of Cardiology,the Affiliated Hospital of North Sichuan Medical College,Nanehong 637000,China)
出处
《中国心血管病研究》
CAS
2018年第9期854-858,共5页
Chinese Journal of Cardiovascular Research
基金
川北医学院校级科研发展计划重点项目(项目编号:CBY16-A-ZD10)
