a School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, 250 Wu-Hsing Street, Taipei 11031, Taiwan.
b Institute of Food Bioresources Technology, Dedan Kimathi University of Technology, P.O. Box 657-10100, Nyeri, Kenya.
Appl Physiol Nutr Metab. 2018 Jul;43(7):669-676. doi: 10.1139/apnm-2017-0670. Epub 2018 Jan 29.
Vascular endothelial dysfunction is a potential risk factor for cardiovascular disease. This study evaluated the effect of curcumin on factors associated with vascular dysfunction using rats fed a high-sucrose, high-fat (HSF) diet. The experiment included 2 animal feeding phases. In the first feeding phase, male Sprague-Dawley rats were randomly divided into 2 groups: the control group (n = 8) was fed a standard diet (AIN-93G) and the HSF group (n = 24) was fed an HSF diet for 8 weeks to induce obesity. In the second feeding phase, lasting 4 weeks, the HSF group was randomly divided into 3 subgroups: the O group (n = 8) continued feeding on the HSF diet, the OA group (n = 8) had the HSF diet replaced with AIN-93G, and the OC group (n = 8) was fed the HSF diet supplemented with curcumin (300 mg/kg body weight daily). After 8 weeks, the HSF diet significantly elevated levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), insulin, homeostatic model assessment insulin resistance (HOMA-IR), low-density lipoprotein cholesterol (LDL-C), homocysteine (Hcy), C-reactive protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhesion molecule 1 (ICAM-1) but significantly reduced levels of nitric oxide (NO) and high-density lipoprotein cholesterol (HDL-C). After dietary intervention, the OA and OC groups exhibited significantly lower levels of AST, ALT, HOMA-IR, cholesterol, LDL-C, Hcy, CRP, VCAM-1, and ICAM-1 and higher levels of NO and catalase (CAT) activity compared with the O group. Superoxide dismutase, CAT, and glutathione peroxidase activities were increased in the OA group, while CAT levels were enhanced in the OC group. In conclusion, this study showed that curcumin supplementation and diet modification can inhibit HSF diet-induced vascular dysfunction potentially by enhancing NO production and antioxidant enzyme activities, thereby suppressing inflammation and oxidative damage in the vascular endothelium.
血管内皮功能障碍是心血管疾病的潜在危险因素。本研究采用高蔗糖高脂肪（HSF）饮食喂养大鼠，评估姜黄素对血管功能障碍相关因素的影响。实验包括 2 个动物饲养阶段。在第一个饲养阶段，雄性 Sprague-Dawley 大鼠随机分为 2 组：对照组（n = 8）喂食标准饮食（AIN-93G），HSF 组（n = 24）喂食 HSF 饮食 8 周以诱导肥胖。在第二个饲养阶段，持续 4 周，HSF 组随机分为 3 个亚组：O 组（n = 8）继续喂食 HSF 饮食，OA 组（n = 8）用 AIN-93G 替换 HSF 饮食，OC 组（n = 8）喂食 HSF 饮食补充姜黄素（每天 300mg/kg 体重）。8 周后，HSF 饮食显著升高天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、胰岛素、稳态模型评估胰岛素抵抗（HOMA-IR）、低密度脂蛋白胆固醇（LDL-C）、同型半胱氨酸（Hcy）、C 反应蛋白（CRP）、血管细胞黏附分子 1（VCAM-1）和细胞间黏附分子 1（ICAM-1），显著降低一氧化氮（NO）和高密度脂蛋白胆固醇（HDL-C）水平。膳食干预后，OA 组和 OC 组的 AST、ALT、HOMA-IR、胆固醇、LDL-C、Hcy、CRP、VCAM-1 和 ICAM-1 水平显著低于 O 组，NO 和过氧化氢酶（CAT）活性显著升高。OA 组超氧化物歧化酶、CAT 和谷胱甘肽过氧化物酶活性增加，OC 组 CAT 水平升高。综上所述，本研究表明，姜黄素补充和饮食调整可能通过增强 NO 生成和抗氧化酶活性来抑制 HSF 饮食诱导的血管功能障碍，从而抑制血管内皮的炎症和氧化损伤。
