Aim:Advanced glycation endproducts(AGE)have been implicated in the patho-genesis of diabetic complications,including diabetic cardiovascular dysfunction.3-[2-(4-Bromo-phenyl)-1-methyl-2-oxo-ethyl]-4,5,6,7-tetrahydro-benzothiazol-3-iumbromide(C16),a novel AGE breaker,was investigated for its effects on the deve-lopment of cardiovascular disease in diabetic rats.Methods:Rats that hadstreptozotocin-induced diabetes for 12 weeks were divided into groups receivingC 16 or vehicle by gavage.Results:In hemodynamic studies of the left ventricle,C16 treatment(25 or 50 mg/kg)for 4 weeks resulted in a significant increase in leftventricular systolic pressure,+dp/dt_(max),and-dp/dt_(max)as compared with vehicle-treated diabetic rats.Furthermore,in hemodynamic studies of the cardiovascularsystem,C16(12.5,25,or 50 mg/kg)treatment for 4 weeks resulted in a dose-dependent and significant increase in cardiac output,a reduction of total periph-eral resistance,and an increase in systemic arterial compliance when comparedwith vehicle-treated diabetic rats.Biochemical studies showed that C16 treatmentalso resulted in a significant decrease in immunoglobulin G-red blood cell surfacecrosslink content and an increase in collagen solubility.Morphological and im-munohistochemical examinations indicated that C 16 was able to prevent increasesof the collagen type Ⅲ/Ⅰ ratio in the aorta and decrease the accumulation of AGEin the aorta.Conclusion:C16 has the ability to reduce AGE accumulation intissues in vivo,and can restore diabetes-associated cardiovascular disorders inrats.This provides a potential therapeutic approach for cardiovascular diseaseassociated with diabetes and aging in humans. Aim: Advanced glycation endproducts (AGE) have been implicated in the patho-genesis of diabetic complications, including diabetic cardiovascular dysfunction. 3- [2- (4-Bromo-phenyl) -1-methyl-2-oxo-ethyl] , 5,6,7-tetrahydro-benzothiazol-3-iumbromide (C16), a novel AGE breaker, was investigated for its effects on the deve-lopment of cardiovascular disease in diabetic rats. Methods: Rats that had streptozotocin-induced diabetes for 12 weeks were divided into groups receiving C 16 or vehicle by gavage. Results: In hemodynamic studies of the left ventricle, C16 treatment (25 or 50 mg / kg) for 4 weeks resulted in a significant increase in left ventricular systolic pressure, + dp / dt_ ( , and-dp / dt max (max) as compared with vehicle-treated diabetic rats. Frthermore, in hemodynamic studies of the cardiovascularsystem, C16 (12.5,25, or 50 mg / kg) treatment for 4 weeks resulted in a dose- dependent and significant increase in cardiac output, a reduction of total periph-eral resistance, and an increase in systemic arterial complian biochemistry studies showed that C16 treatment also resulted in a significant decrease in immunoglobulin G-red blood cell surface cross-link content and an increase in collagen solubility. Morphological and im-munohistochemical examinations indicated that C 16 was able to prevent increasesof the collagen type Ⅲ / Ⅰ ratio in the aorta and decrease the accumulation of AGEin the aorta. Confclusion: C16 has the ability to reduce AGE accumulation intissues in vivo, and can restore diabetes-associated cardiovascular disorders in patients. This provides a potential therapeutic approach for cardiovascular diseaseassociated with diabetes and aging in humans.