心臟衰竭是全球心血管疾病最後高死亡率的原因之一。其中一造成心臟衰竭原因包含治療癌症患者所使用的化學治療藥物。阿黴素是一治療癌症的有效化療藥物，但也有報告指出阿黴素可以誘發心肌病，最終產生心臟衰竭。利用高劑量阿黴素引起心臟衰竭的小鼠是一種常用的動物模型來探討治療心臟衰竭手段，包括：藥物、細胞、器械或蛋白的作用機轉。在心臟和心肌病的過程中，炎症反應很容易發生。 C/EBP δ 屬於 CCAAT/增強子結合蛋白 (CCAAT / Enhancing Binding Protein: C/EBP) 家族的轉錄因子，在正常狀態細胞中是低的，當受到外來刺激物質的影響會快速被誘發，進而引發細胞內一系列訊號傳導。一些報告提出了 C / EBP δ，在先天免疫反應的激活作用，也是促進炎症反應。根據過去細胞與實驗動物研究指出，C / EBP δ 缺乏可能防止脂多醣 (LPS) 誘導的肺損傷，但對 C/ EBP δ 於心肌細胞的作用, 只限於有限的研究資料。在我們的研究中，利用腹腔注射阿黴素誘導在小鼠心臟產生的慢性炎症反應，並利用現有的 Cebpd 基因剔除鼠，研究心臟衰竭的病理生理過程中 C / EBP δ 所扮演的作用。我們發現，剔除 C/EBP δ 可以降低使用阿黴素的初期對心臟造成的傷害，並且提高小鼠的存活率．未來也許可以應用在慢性及急性心臟衰竭的患者，於初期抑制 C/EBP δ 並合併抗發炎藥物降低心肌發炎的因素，降低治療前及治療中，心臟受損的機率，提升更穩定及增加治療機會．

Heart failure (HF) is one of the leading causes of cardiovascular mortality and morbidity in the world. In the treatment of cancer patients, the chemical used in chemotherapy, doxorubicin (DOX), can induce cardiomyopathy and HF. DOX-induced HF in mice is a commonly used animal model to explore the mechanism and therapeutic tools. During the process of cardiotoxicity and cardiomyopathy, inflammation reactions occur. C/EBP δ belongs to the CCAAT/enhancer binding protein (C/EBP) family of transcription factors, and it is low in normal physiological conditions but will rapidly increase in number from certain external stimuli, inducing signal transduction in the cell. Some reports have suggested a role for C/EBP δ in the activation of the innate immune response and pro-inflammatory conditions. It regulates the expression of inflammatory genes. Previous studies have shown that Cebpd deficiency could protect against lipopolysaccharide (LPS)-induced lung injury in vivo, however, few studies have examined the role of C/EBP δ on cardiomyocytes. In our study, intraperitoneal (i.p.) injections DOX induced chronic inflammation reaction in mice heart. Using cebpd knockout mice to test the role of C/EBP δ during the pathophysiologic course of HF. We found that cebpd deficiency could reduce HF in the early stage while DOX treatment and improve the chance of survival. In the future, it may combine the inhibition of C/EBP δ with anti-inflammatory drugs to reduce the myocardial inflammatory responses in the chronic/acute HF patients. It will ameliorate the heart injury in the early treatment and improve the more stable and healing opportunity.

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