The Protective Effects of Ivabradine in Preventing Progression from Viral Myocarditis to Dilated Cardiomyopathy.
The Protective Effects of Ivabradine in Preventing Progression from Viral Myocarditis to Dilated Cardiomyopathy.
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伊伐布雷定预防病毒性心肌炎进展为扩张型心肌病的保护作用
DOI：
10.3389/fphar.2016.00408
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发表时间：
2016
影响因子：
5.6
通讯作者：
Xiangjun Y
中科院分区：
文献类型：
--
作者：
Yue-Chun L;Guang-Yi C;Li-Sha G;Chao X;Xinqiao T;Cong L;Xiao-Ya D;Xiangjun Y
研究伊伐布雷定对扩张型心肌病 (DCM) 小鼠的有益作用，该病是由柯萨奇病毒 B3 诱导的慢性病毒性心肌炎演变而来。 4-5周龄雄性balb/c小鼠在第1、14和28天腹腔内接种柯萨奇病毒B3（Nancy株）。第一次接种病毒的当天定义为第1天。35天后，将存活的慢性病毒性心肌炎小鼠随机分为两组，治疗组和未治疗组。治疗组伊伐布雷定连续灌胃30 d，未治疗组给予生理盐水。采用Masson三色染色评价心肌组织纤维化程度。 Western blot检测肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、白细胞介素-6（IL-6）、Ⅰ型胶原、Ⅲ型胶原、p38-MAPK信号通路蛋白的表达水平。心电图用于检查心率和节律。通过超声心动图检查室间隔和左心室后壁的厚度、左心室舒张末期内径、左心室收缩末期内径、左心室射血分数和缩短分数。与未经治疗的慢性病毒性心肌炎小鼠相比，伊伐布雷定显着提高了小鼠的存活率，减轻了心肌病变和纤维化，改善了左心室功能损伤，缩小了心脏尺寸，减少了I型胶原和III型胶原的产生，减少了促炎细胞因子TNF-α、IL-1β和IL-6的表达，并降低了磷酸-p38 MAPK的产生。研究结果表明，伊伐布雷定在预防柯萨奇病毒 B3 诱导的慢性病毒性心肌炎小鼠从病毒性心肌炎进展为 DCM 方面的治疗作用与抑制 p38 MAPK 通路、下调炎症反应和减少胶原蛋白表达有关。伊伐布雷定似乎是治疗病毒性心肌炎患者的一种有前途的方法。
To study the beneficial effects of ivabradine in dilated cardiomyopathy (DCM) mice, which evolved from coxsackievirus B3-induced chronic viral myocarditis. Four-to-five-week-old male balb/c mice were inoculated intraperitoneally with coxsackievirus B3 (Strain Nancy) on days 1, 14, and 28. The day of the first virus inoculation was defined as day 1. Thirty-five days later, the surviving chronic viral myocarditis mice were divided randomly into two groups, a treatment group and an untreated group. Ivabradine was administered by gavage for 30 consecutive days in the treatment group, and the untreated group was administered normal saline. Masson’s trichrome stain was used to evaluate the fibrosis degree in myocardial tissue. The expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), collagen I, collagen III and p38-MAPK signaling pathway proteins were detected by Western blot. Electrocardiogram was used to investigate the heart rate and rhythm. The thickness of the ventricular septum and left ventricular posterior wall, left ventricular end diastolic dimension, left ventricular end systolic dimension, left ventricular ejection fractions and fractional shortening were studied by echocardiography. Compared with the untreated chronic viral myocarditis mice, ivabradine significantly increased the survival rate, attenuated the myocardial lesions and fibrosis, improved the impairment of the left ventricular function, diminished the heart dimension, decreased the production of collagen I and collagen III, reduced the expression of the proinflammatory cytokines TNF-α, IL-1β, and IL-6, and lowered the production of phospho-p38 MAPK. The findings indicate the therapeutic effect of ivabradine in preventing the progression from viral myocarditis to DCM in mice with chronic viral myocarditis induced by coxsackievirus B3, is associated with inhibition of the p38 MAPK pathway, downregulated inflammatory responses and decreased collagen expression. Ivabradine appears a promising approach for the treatment of patients with viral myocarditis.
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影响因子：
37.8
作者：
Eriksson, U;Kurrer, MO;Kopf, M
通讯作者：
Kopf, M
DOI：
10.1186/1755-1536-2-7
发表时间：
2009-12-15
期刊：
Fibrogenesis & tissue repair
影响因子：
--
作者：
Chen CZ;Raghunath M
通讯作者：
Raghunath M
影响因子：
37.8
作者：
Li, MX;Georgakopoulos, D;Wang, YB
通讯作者：
Wang, YB
尼古丁抑制柯萨奇病毒 B3 感染小鼠促炎细胞因子的产生
影响因子：
6.1
作者：
Ge Li-Sha;Zhao Jing-Lin;Li Yue-Chun
通讯作者：
Li Yue-Chun
影响因子：
56.9
作者：
BEERE, PA;GLAGOV, S;ZARINS, CK
通讯作者：
ZARINS, CK