Abstract: Objective To investigate protective effects of astaxanthin（ASX）on endothelial function of aortas in diabetic rats and its possible molecular mechanisms involved. Methods Eighteen rats were randomly selected out of34 male Wistar rats for constructing type 1diabetes model by a single intraperitoneal injection of 1% streptozotocin（STZ）,in which 2rats failed to induce diabetes were excluded. Normal Wistar rats were randomly divided into control group and control rats treated with ASX（30mg/kg）group. Diabetic rats were randomly divided into diabetic group（n=8）and diabetic rats treated with ASX（30mg/kg）group（n=8）. Endothelial function of aorta was examined.Serum oxidized low-density lipoprotein（ox-LDL）level was detected by enzyme-linked immunosorbent assay（ELISA）;the malondialdehyde level（MDA）and superoxide dismutase（SOD）activity in aorta by thiobarbituric acid reactive substance assay（TBARS）and xanthine oxidase methods respectively;and the mRNA and protein expression of lectin-like oxidized low-density lipoprotein receptor-1（LOX-1）in aorta by reverse transcription polymerase chain reaction and Western blot methods. Results Excessive oxidative stress and endothelial dysfunction were found in STZ-induced diabetic rats as indicated by increased serum ox-LDL （4.64±0.55）vs（2.64±0.18）μg/dL,P＜0.05,increased aortic MDA （3.38±0.22）vs（2.04±0.27）nmol/mg pro,and impaired endothelium-dependent vasorelaxation to acetylcholine（Ach）. Simultaneously,the mRNA and protein expression of LOX-1were enhanced while eNOS expression reduced in the aortas of diabetic rats. ASX treatment could alleviate those manifestations by decreasing serum ox-LDL （2.96±0.25）vs（4.64±0.55）μg/dL,P＜0.01and aortic MDA （2.04±0.17）vs（3.38±0.22）nmol/mg pro,P＜0.01,by improving endothelium-dependent vasodilator responses to ACh,and by upregulating eNOS while down-regulating LOX-1expression. Conclusion ASX could downregulate ox-LDL and LOX-1expressions,upregulate the eNOS expression,and ameliorate the endothelial dysfunction in diabetic rats.