الفهرس 
Aim of the studyOnly 14 pages are availabe for public view
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Abstract
Myocardial infarction, more commonly known as a heart attack, is the primary cause of cardiovascular mortality and accounts for approximately one-third of cases of congestive heart failure. After myocardial infarction, an estimated 35% of patients develop heart failure within a span of five years because of chronically ischemic heart injury. Granulocyte colony-stimulating factor (G-CSF) has captured the attention of researchers over the last 20 years as an essential therapeutic treatment. It is a glycoprotein found in numerous bodily tissues. It has the potential to promote cell survival, mobilization, and proliferation. It stimulates the formation of various precursors in the bone marrow, such as granulocytes and stem cells, and then releases them into the bloodstream. It inhibits the production of pro-inflammatory cytokines. G-CSF has been shown to improve heart function, stabilize myocardial electrophysiological characteristics, prevent ventricular remodeling, reduce myocardial apoptosis and inflammation, and reduce the risk of ventricular arrhythmia during ischemia reperfusion injury.
Galangin is a polyphenolic substance extracted from the ginger plant galangal. Galangin has been proven in previous research to reduce cell proliferation, promote apoptosis, prevent cancer cell metastasis, induce cell autophagy, and provide anti-inflammatory and antioxidant properties. According to recent research, it plays a crucial part in the process of neointimal hyperplasia after vascular damage.
The ISP-induced myocardial ischemia model is a simple, noninvasive, cost-effective, and time-efficient method of inducing MI that leaves the pericardium intact. As previously described, ISP delivery regularly results in cardiac dysfunction and left ventricular dilatation like that seen in the extensively infarcted heart.
The purpose of this study is to investigate the histological responses to G-CSF versus Galangin on isoproterenol-mediated cardiotoxicity.