Total Flavones of Choerospondias axillaris Attenuate Cardiac Dysfunction and Myocardial Interstitial Fibrosis by Modulating NF-κB Signaling Pathway
Total Flavones of Choerospondias axillaris Attenuate Cardiac Dysfunction and Myocardial Interstitial Fibrosis by Modulating NF-κB Signaling Pathway
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DOI：
10.1007/s12012-014-9298-3
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发表时间：
2015-07-01
影响因子：
3.2
通讯作者：
Gao, Zhiyong
中科院分区：
文献类型：
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作者：
Sun, Bei;Xia, Qiumei;Gao, Zhiyong
本研究旨在探讨酸枣总黄酮（TFC）对心肌梗死（MI）引起的心功能障碍、间质纤维化和炎症反应的影响，并进一步阐明其潜在的信号通路。通过冠状动脉闭塞使大鼠遭受心肌梗死。以心电图出现ST段抬高证实模型建立。然后，连续28天（灌胃）施用TFC，剂量为75、150和300mg/kg。记录体重和心脏重量。检查血流动力学、梗塞面积和心肌纤维化。收集血样以确定肿瘤坏死因子-α (TNF-α) 和白细胞介素 6、10 (IL-6、IL-10) 水平。通过Western blot检测基质金属蛋白酶2、9（MMP-2、9）、磷酸化IKBα（p-IKBα）和转化生长因子β1（TGF-β1）的表达。结果表明，TFC显着改善MI大鼠的心功能障碍、心脏系数和心肌纤维化。 TFC 还降低了 TNF-α 和 IL-6 的水平，但增加了 IL-10 的含量。此外，TFC 治疗可通过降低 MMP-2、9、TGF-β 1 和 p-IKB α 的表达来保护心脏免受慢性 MI 损伤。结果表明，TFC 通过调节核因子-κ B (NF-κ B) 信号通路减轻心脏功能障碍和心肌间质纤维化。
This study aimed to investigate the effect of total flavonoids of Choerospondias axillaris (TFC) on myocardial infarction (MI)-induced cardiac dysfunction, interstitial fibrosis and inflammatory reaction and further to clarify the potential signaling pathway involved. Rats were subjected to MI via coronary artery occlusion. The model establishment was confirmed by the occurrence of ST-segment elevation in electrocardiogram. Then, TFC was administrated at doses of 75, 150 and 300 mg/kg for 28 consecutive days (gavage). Body weight and heart weight were recorded. Hemodynamics, infarct size and myocardial fibrosis were examined. Blood samples were collected to determine tumor necrosis factor-alpha (TNF-alpha) and interleukin 6, 10 (IL-6, IL-10) levels. The expressions of matrix metalloproteinases-2, 9 (MMP-2, 9), phosphor-IKB alpha (p-IKB alpha) and transforming growth factor-beta 1 (TGF-beta 1) were assayed by Western blot. The results indicated that TFC significantly improved cardiac dysfunction, the heart coefficient and myocardial fibrosis in MI rat. TFC also decreased the levels of TNF-alpha and IL-6, but increased IL-10 content. Moreover, treatment with TFC protected the heart from chronic MI injury by decreasing the expressions of MMP-2, 9, TGF-beta 1 and p-IKB alpha. The results suggested that TFC attenuated cardiac dysfunction and myocardial interstitial fibrosis by modulating nuclear factor-kappa B (NF-kappa B) signaling pathway.