阿霉素诱导小鼠急性心肌损伤模型的动态研究及心血康的保护作用OA

Objective:This study aims to elucidate the temporal pathological progression and key toxicological mechanisms of Doxorubicin(DOX)-induced acute myocardial injury in mice,and to evaluate the pharmacological effects of Xinxuekang(XXK),thereby providing an experimental basis for the prevention and treatment of DOX-induced acute cardiotoxicity.Methods:An acute myocardial injury model in Kunming mice through intraperitoneal injection of DOX and assessed cardiac injury was es-tablished.Enzyme assay,HE staining,TEM,and transcriptome profiling were performed to dynamically assess myocardial injury and the effects of XXK.Results:DOX markedly increased serum CK-MB and LDH levels on day 2.Histopathology revealed early vacuolisation and inflammatory infiltration,progressing to fibre disarray and interstitial oedema on days 4 and 6,and marked cytoplasmic vacuolisation with nuclear pyknosis and fragmentation on day 8.TEM demonstrated progressive mitochondrial swell-ing,cristae disruption,and membrane injury on day 4 and 8.Transcriptomic analysis indicated activation of cellular stress path-ways in the early phase,followed by repair and adaptive responses.XXK administration mitigated enzyme elevation,preserved mitochondrial integrity,and alleviated pathological damage.Conclusion:Early DOX-induced cardiotoxicity is characterised by cellular oedema,mitochondrial dysfunction,and oxidative stress,whereas later stages reflect compensatory repair.Early XXK in-tervention confers significant protection against acute DOX-induced myocardial injury.