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敦煌疗风虚瘦弱方对大鼠慢性心衰的治疗作用及其机制     被引量:2

Therapeutic effects of Dunhuang Liaofengxushouruo decoction on chronic heart failure in rats

文献类型:期刊文献

中文题名:敦煌疗风虚瘦弱方对大鼠慢性心衰的治疗作用及其机制

英文题名:Therapeutic effects of Dunhuang Liaofengxushouruo decoction on chronic heart failure in rats

作者:吴国泰[1,2];杜丽东[2];陈振鹤[2];蔺兴遥[1,2];李金田[1,2];李芳[2]

第一作者:吴国泰

机构:[1]甘肃中医药大学敦煌医学与转化省部共建教育部重点实验室,兰州730000;[2]甘肃中医药大学甘肃省中药药理与毒理学重点实验室,兰州730000

第一机构:甘肃中医药大学科研实验中心(甘肃省中医药标准化技术委员会秘书处)

年份:2017

卷号:33

期号:6

起止页码:558

中文期刊名:中国应用生理学杂志

外文期刊名:Chinese Journal of Applied Physiology

收录:CSTPCD;;Scopus;CSCD:【CSCD2017_2018】;PubMed;

基金:敦煌医学与转化省部共建教育部重点实验室开放基金(DHYX1212-010);2015年甘肃省“陇原青年创新人才扶持计划”项目(2015-003)

语种:中文

中文关键词:敦煌疗风虚瘦弱方;慢性心力衰竭;阿霉素;心肌损伤,血流动力学;大鼠

外文关键词:Dunhuang Liaofengxushoumo decoction; chronic heart failure; adriamycin; myocardial injury; hemodynamics; rats

摘要:目的:观察敦煌疗风虚瘦弱方(LXD)对慢性心衰大鼠的治疗作用及机制。方法:48只Wistar雄性大鼠随机分为6组(n=8):正常组、模型组、卡托普利组和LXD高、中、低剂量组。除正常组外,其余各组大鼠尾静脉注射阿霉素(2.5 mg/kg),每周1次,连续6周复制慢性心衰模型,末次注射阿霉素60 min后,卡托普利组灌胃卡托普利,LXD高、中、低剂量组分别以灌胃LXD水煎液80、40、20 g/kg(生药/体重),正常组和模型组灌胃等容量生理盐水,每天1次,连续6周,同时每周腹腔注射15 mg/kg异丙肾上腺素1次。记录各组大鼠的呼吸、皮毛颜色、活动、体重、力竭游泳时间、心率(HR)、平均动脉压(MAP)、左室收缩压(LVSP)、左室舒张末压(LVEDP)、左室内压最大上升速率(+dp/dtmax),左室内压最大下降速率(-dp/dtmax),检测血清白介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)水平,评价抗氧化活性和心室质量指数,光镜下观察心肌组织形态变化。结果:与正常组比较,模型大鼠体重增长减慢,力竭游泳时间明显缩短,心脏功能减弱,出现细胞因子激活、自由基损伤、心肌酶释放增多,HE染色显示心肌组织形态出现损伤,心肌纤维断裂等。与模型组比较,各剂量LXD对模型大鼠有不同程度的治疗作用,给药第42天,LXD各剂量组体重明显增长;LXD高、中剂量组力竭游泳时间明显延长(P<0.05),MAP、血清IL-6、TNF-α、MDA、LVMI和RVMI显著降低(P<0.05,P<0.01),LVSP、+dp/dtmax及-dp/dtmax均显著升高(P<0.05,P<0.01),LXD高剂量组LVEDP显著降低(P<0.01),LXD中、低剂量组CK和AST显著降低(P<0.05,P<0.01);LXD各剂量组血清SOD升高。结论:敦煌疗风虚瘦弱方对阿霉素诱导的慢性心衰模型大鼠具有一定的治疗作用,作用机制与改善血流动力学,降低心肌组织损伤有关。
Objective; To observe the therapeutic effects and mechanism of Dunhuang Liaofengxushouruo decoction (LXD) (Traditional Chinese Medicine) on ehronic heart failure(CHF) in rats. Methods: Forty-eight male Wistar rats were randontly divided into normal group( n = 8) :model group, eaptopril group and IXD(Traditional Chinese Medicine) high, medium and low dose group. Except the nonnal group, the rats were intravenous injected with adriamycin 2.5 mg/kg in one day for 6 weeks, the captopril rats were intragastrie administrated hy captopril 25 mg/kg, I,XD high, medium arid low dose groups were intragastrie administrated by LXD d 80, 40, 20 g/kg for 6 consecutive weeks. The rats breathing, coat color, aetivity, body weight(BW) and time of exhaustive swimming were measured; Heart rate, mean arterial pressure (MAP), left ventrieular systolic pressttre (LVSP), left ventrieular end diastolic pressure (LVEDP), maximal rate of left veutricular pressure ( + dp/dtmax or -dp/dtmax)of each rat were examined by Power Lab. The levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were measured; The rats were sacrificed and hearts removed fur separation of lelt and right ventricle, the antioxidant activity and ven- tricular mass index were measured, left ventricular myocardium was administrated by 4% parafomlaldehyde, HE staining, morphological changes were observed under microscope. Results: Body weight of each group decreased, and time of exhaustive swimming decreased 'after modeling ( P 〈 0.01 ). At 28 days after administration, BW in high and middle dose of LXD groups were inerea,sed and the swimming time of rats in LXD high dose group was increased ( P 〈 0.05). At 42 days , BW in all of LXD groups were increased and the exhaustive swimming time of high and middle dose of LXD were prolonged ( P 〈 0.05), MAP was decreased and LVSP, + dp/dtmax or -dp/dtmax were increased in IXD high and middle groups. The LVEDP was decreased in high dose of LXD group( P 〈 0.05, P 〈 0.01 ). The levels of ereatine kinase (CK) and aspartate anfinotransferase (AST) in middle and low dose of IXD groups were decreased( P 〈 0.05, P 〈 0.01), and the serum lev- els of IL-6, TNF-a and malondialdehyde (MDA) in serum in IXD high and middle dose groups were lower. The activities of supemxide dismu- tase (SOD) in serum were inereased in all of LXD groups, and the LVMI and RVMI were decreased in high and middle dose of LXD groups( P 〈 0.05, P 〈 0.01 ). The pathological results showed that myocardial fiber arrangement and myocardial interstitial edema phenomenon were obviously improved in high dose of LXD group and CMD decreased. Conclusion: Therapeutic effect of LXD on CHF by doxorubicin-induced in rats is confirmed, the mechanisms are associated with improved hemodynamics and myocardial tissue.

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