Podium 01
應用肉桂醛對大鼠第一型心腎症候群模式之心腎病理緩解作用之探討
鄭瑀萱1,2、鄭劍廷1、林威佑1,2
1國立臺灣師範大學生命科學院、 2衛生福利部臺北醫院泌尿科
To evaluate the effect of Cinnamaldehyde on the cardiac and renal pathology in a rat model of cardiorenal syndrome type 1.
Yu-Hsuan Cheng1,2、Chiang-Ting Chien1、Wei-Yu Lin1,2
1 Department of Life Science, National Taiwan Normal University, Taipei, Taiwan
2Department of Urology,Taipei Hospital, Ministry of Health and Welfare, New Taipei City, Taiwan
Purpose:
Cardiorenal syndrome (CRS) encompasses a spectrum of disorders involving both the heart and kidneys in which acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. CRS is divided into five subtypes of which CRS type 1 (CRS1) is the most common. CRS1, also known as acute CRS, refers to acute worsening of heart function leading to kidney injury and/or dysfunction. It is commonly seen after a patient experiences cardiac surgery, acute heart failure or an acute coronary syndrome such as acute myocardial infarction. New findings suggest Bcl-2–associated athanogene 3 (BAG3) may provide a therapeutic target in patients undergoing reperfusion after myocardial infarction. Accumulating evidence demonstrate that Cinnamaldehyde therapy exerts beneficial effects in the cardiovascular diseases, such as viral myocarditis, ischemic heart disease, atherosclerosis and cardiac hypertrophy. This study identified that cardioprotective effect and renal protection of BAG3 regulation by 2‘-Hydroxycinnamaldehyde (HCA) from myocardial ischemia/reperfusion (I/R) injury induced CRS type 1.
Materials and Methods:
Male Wistar rats were subjected to 60 min of ischemia by occlusion of the left anterior descending coronary artery followed by 240 min reperfusion. This CRS1 model in the present study was induced by a cardiac I/R injury model in rodents leading to acute kidney injury. Animals were randomly assigned into a sham control (Sham group), I/R injury (I/R group), and pre-treatment of HCA with I/R injury (HCA+I/R group).
Cardiac function was determined with hemodynamic parameters, electrocardiogram, microcirculation, immunohistochemistry and infarct size. Renal function was determined with biochemistry and immunohistochemistry.
Results:
Our preliminary data have displayed several parameters in the CRS1 model by ligation of coronary arterial circulation in the rat implicating the successful induction of cardiac I/R injury. I/R injury increased ST segment elevation, left ventricular end-diastolic pressure (LVEDP) level, infarct size, erythrocyte accumulation and leukocyte infiltration in the cardiac phenotype, and increased plasma creatinine, blood urea nitrogen (BUN), urine protein and renal fibrosis, including severe glomerular damage and tubular dilation in renal histology. HCA treatment significantly reduced the above parameters of the cardiac and renal dysfunction.
Conclusion:
This study aims to explore the undefined mechanisms and the incorporation of available drugs and/or biomarkers to reduce cardiac and kidney injury and to guide therapeutic strategies in CRS. Our results suggest that HCA could be a potentially therapeutic drug to attenuate cardiac I/R injury induced acute renal dysfunction.