摘要标题:

通过上调的SMAD7抑制TGF-β/Smad信号传导小鼠的MI-Emodin在小鼠中改善了心脏重塑。

摘要来源:

phytomedicine。 2023 Jun; 114:154793。 EPUB 2023 3月30日。PMID: 37011420“> 37011420 Wen Li,Yunqi Liu,Jiapan Wang,Jia Wang,Yilian Yang,Yan Hao,Zhen Liang,Zhen Liang,Yiping Tao,Ye Yuan,Ye Yuan,Zhimin du

文章隶属关系:

(AE)是一种自然中国药用植物的天然蒽醌提取物,已获得证明可预防急性心肌缺血。然而,它对慢性心肌梗塞(MI)后对心脏重塑的影响且可能的机制尚不清楚。

ascor: 这项研究研究了效果o o o o o of AE on cardiac remodeling and oxidative damage induced by myocardial infarction (MI) in vitro and explored the underlying mechanisms.

METHODS: Echocardiography and Masson staining were used to demonstrate myocardial dysfunction and fibrosis.通过TUNEL染色检测到细胞凋亡。 The expressions of fibrosis-related factors such as type I collagen,α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) were detected by Western blot.

RESULTS: Our data demonstrated that AE treatment significantly improved cardiac function, reduced structural remodeling, and患有心肌梗塞的小鼠的心脏凋亡和氧化应激减少。在体外,AE可以保护新生小鼠心肌细胞(NMCM)免受血管紧张素II(ANG II)诱导的心肌细胞肥大和凋亡,并显着抑制(P <0.05)Ang II诱导的活性氧物种(ROS)增加。 Furthermore, AE treatment significantly reversed the Ang ii-induced upregulation.

CONCLUSION: In summary, our work reveals for the first time that AE activates the TGF-βsignaling pathway by up-regulating Smad7 expression, which in turn regulates the expression of fibrosis-related genes,最终改善心脏功能,抑制慢性MI大鼠心脏纤维化和肥大的发展。

研究类型 : 动物研究
更多链接
疾病 : 心肌梗塞,
治疗物质 : 大黄素,

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