Abstract: AIM To observe the aggravating mechanism of myocardial injury in aging individuals after mechanical trauma, especially the role of advanced glycosylation end products. METHODSA mechanical trauma mice model was established in C57 male mice by Noble-Collip drum. C57 adult mice (2 months) and aged C57 mice (20 months) were randomized into non-trauma group, trauma group and intervention group. Left ventricular ejection fraction and left ventricular short axis shortening rates were detected using color Doppler ultrasonographic diagnosis apparatus. Expressions of AMP protein kinase (p-AMPK), AMP protein kinase (AMPK), p53 and p16 were analyzed by Western blot. Soluble advanced glycosylation end products (sRAGE) and carboxymethyllsine (CML) were detected by ELISA kits. RESULTSCompared with control group (adult mice), myocardial injury in elderly mice significantly increased after mechanical trauma. Left ventricular ejection fraction and left ventricular short axis shortening rate were significantly lower (P<0.01). MG-AGEs significantly increased after mechanical trauma (P<0.05) and AMPK activity declined (P<0.05). In-advance intervention with AGEs significantly improved myocardial function in elderly mice after trauma. CONCLUSIONThe aggravating mechanism of myocardial injury in aging individuals after mechanical trauma is associated with MG-AGEs system. MG-AGEs system may be an effective target for clinical treatment in aging patients.