Progression of heart failure is attenuated by antioxidant therapy with N-acetylcysteine in myocardial infarcted female rats
Progression of heart failure is attenuated by antioxidant therapy with N-acetylcysteine in myocardial infarcted female rats
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DOI：
10.1007/s11033-020-05907-4
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发表时间：
2020-10-13
影响因子：
2.8
通讯作者：
Olivares, Emerson L.
中科院分区：
文献类型：
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作者：
Costa, Cesar R. M.;Seara, Fernando A. C.;Olivares, Emerson L.
本研究探讨了N-乙酰半胱氨酸（NAC）在治疗雌性大鼠心力衰竭中的治疗潜力。心肌梗塞（MI）大鼠给予NAC（250 mg/kg/天p.o.）在手术后28天期间，给予MI + NAC或溶媒（MI +安慰剂），并且假手术大鼠接受相同的处理（假手术+ NAC和假手术+安慰剂）。在治疗的最后一周进行心电图和超声心动图分析。评估I型和II型超氧化物歧化酶（SOD）、过氧化氢酶、I型和III型谷胱甘肽过氧化物酶（GPX）、神经生长因子（NGF）、β 1-肾上腺素能受体（β 1ADR）和2型毒蕈碱受体（M2 R）的心脏mRNA水平。评估心脏水平、NADPH氧化酶（NOX）活性（、还原硫醇总含量、SOD、GPX和过氧化氢酶活性）。与MI +安慰剂组相比，MI + NAC组表现出降低的NOX活性、增加的还原巯基含量、增加的GPX活性和正常化的GPX III mRNA水平（p < 0.05）。与MI +安慰剂组相比，MI + NAC组的心和肺重量、左心室（LV）舒张末期容积和左心房/主动脉比降低，而LV后壁厚度和射血分数增加（p < 0.05）。与MI +安慰剂组相比，MI + NAC组低频功率密度降低，高频功率密度和连续差值的均方根增加（p < 0.05）。这些发现表明，NAC促进MI诱导的心力衰竭在雌性大鼠中的进展的治疗效果。
This study investigated the therapeutic potential of N-acetylcysteine (NAC) in the treatment of heart failure in female rats. Myocardial infarcted (MI) rats were given NAC (250 mg/kg/day p.o.) during 28 days after surgery (MI + NAC) or vehicle (MI + Placebo), and sham-operated rats received the same treatments (Sham + NAC and Sham + Placebo). Electrocardiographic and echocardiographic analyses were performed in the last week of treatment. Cardiac mRNA levels of types I and II superoxide dismutase (SOD), catalase, types I and III glutathione peroxidase (GPX), nerve growth factor (NGF), beta 1-adrenergic receptor (beta 1ADR), and type 2 muscarinic receptor (M2R) were assessed. Cardiac levels NADPH oxidase (NOX) activity(,)total content of reduced thiols, and SOD, GPX, and catalase activity were assessed. Compared to MI + Placebo group, MI + NAC group exhibited decreased NOX activity, increased content of reduced thiols, increased GPX activity, and normalized GPX III mRNA levels (p < 0.05). Heart and lung weights, left ventricular (LV) end-diastolic volume and left atrium/aorta ratio were decreased, while LV posterior wall thickness and ejection fraction were increased in MI + NAC group versus MI + Placebo rats (p < 0.05). Power density of low frequency band was decreased, while power density of high frequency and the root mean square of the successive differences were increased in MI + NAC rats versus MI + Placebo (p < 0.05). These findings indicate that NAC promotes therapeutic effects in the progression of MI-induced heart failure in female rats.