scholarly journals Resveratrol Pretreatment Inhibits Myocardial Apoptosis in Rats Following Coronary Microembolization via Inducing the PI3K/Akt/GSK-3β Signaling Cascade

2021 ◽  
Vol Volume 15 ◽  
pp. 3821-3834
Author(s):  
Tao Li ◽  
Zhiqing Chen ◽  
You Zhou ◽  
Haoliang Li ◽  
Jian Xie ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Qiang Su ◽  
Xiangwei Lv ◽  
Ziliang Ye

Background/Aims. Coronary microembolization- (CME-) induced myocardial injury and progressive cardiac dysfunction are mainly caused due to CME-induced myocardial local inflammatory response and myocardial apoptosis. Ligustrazine plays an important protective role in multiple cardiovascular diseases, but its role and the protection mechanism in CME is unclear. This study hypothesized that ligustrazine attenuates CME-induced myocardial injury in rats. This study also explored the mechanism underlying this attenuation. Methods. Forty SD rats were randomly divided into CME group, ligustrazine group, ligustrazine+LY294002 (ligustrazine+LY) group, and sham group (ten rats in each). In each group, the cardiac function, apoptotic index, serum c-troponin I (cTnI) level, inflammation [interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α)], and oxidative stress [nitric oxide (NO), superoxide dismutase (SOD), and malondialdehyde (MDA)] were determined. Western blotting was used to detect the proteins which are present in the PI3K/Akt pathway. Results. Ligustrazine improved cardiac dysfunction induced by CME, increased serum NO and SOD activities, and decreased the serum level in IL-1β, MDA, cTnI, and TNF-α. Moreover, ligustrazine inhibited myocardial apoptosis, which is perhaps caused by the upregulated Bcl-2, the downregulated cleaved caspase-3 and Bax, and the increased protein level in endothelial nitric oxide synthase and phosphorylated Akt. These effects, however, were reduced if ligustrazine was coadministered with LY294002. Conclusions. Ligustrazine attenuates CME-induced myocardial injury. The effects associated with this attenuation may be achieved by activating the myocardium PI3K/Akt signaling pathway.


APOPTOSIS ◽  
2009 ◽  
Vol 14 (11) ◽  
pp. 1299-1307 ◽  
Author(s):  
Jun-Qiu Song ◽  
Xu Teng ◽  
Yan Cai ◽  
Chao-Shu Tang ◽  
Yong-Fen Qi

2011 ◽  
Vol 61 (2) ◽  
pp. 399-406 ◽  
Author(s):  
Lang Li ◽  
Qiang Su ◽  
Yan Wang ◽  
Rixin Dai ◽  
Yongguang Lu ◽  
...  

2016 ◽  
Vol 22 (2) ◽  
pp. 189-195
Author(s):  
Jiang-You Wang ◽  
Han Chen ◽  
Xi Su ◽  
You Zhou ◽  
Lang Li

Background/Aim: In addition to its cholesterol-lowering effect, atorvastatin (ATV) has been thought to have multiple cardiovascular benefits, including anti-inflammatory and anti-apoptotic properties. The present study was undertaken to determine whether ATV pretreatment could attenuate myocardial apoptosis and inflammation and improve cardiac function in a swine model of coronary microembolization (CME). Methods: Twenty-four swine were randomly and equally divided into a sham-operated (control) group, CME group, and CME plus ATV group. Swine CME was induced by intracoronary injection of inert plastic microspheres (diameter 42 μm) into the left anterior descending coronary, with or without pretreatment of ATV. Echocardiographic measurements, a pathological examination, terminal deoxynucleotidyl transferase–mediated nick end labeling staining, and Western blotting were performed to assess the functional, morphological, and molecular effects in CME. Results: The expression levels of caspase 3 and tumor necrosis factor-α (TNF-α) were aberrantly upregulated in cardiomyocytes following CME. Downregulation of caspase 3 and TNF-α with ATV pretreatment was associated with improved cardiac function and attenuated serum cardiac troponin I (cTnI) and high-sensitivity C-reactive protein. In addition, through a Pearson correlation analysis, the left ventricular ejection fraction negatively correlated with caspase 3, TNF-α, and cTnI. Conclusion: This study demonstrated that ATV pretreatment could significantly inhibit CME-induced myocardial apoptosis and inflammation and improve cardiac function. The data generated from this study provide a rationale for the development of myocardial apoptosis and inflammation-based therapeutic strategies for CME-induced myocardial injury.


APOPTOSIS ◽  
2009 ◽  
Vol 14 (9) ◽  
pp. 1061-1069 ◽  
Author(s):  
Jun-Qiu Song ◽  
Xu Teng ◽  
Yan Cai ◽  
Chao-Shu Tang ◽  
Yong-Fen Qi

2013 ◽  
Vol 4 (2) ◽  
pp. 138 ◽  
Author(s):  
Qiang Su ◽  
Lang Li ◽  
Yang-chun Liu ◽  
You Zhou ◽  
Wei-ming Wen

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