Department of Biochemistry, CSIR-Central Food Technological Research Institute, Mysore, Karnataka, 570 020, India.
Department of Molecular Nutrition, CSIR-Central Food Technological Research Institute, Mysore, Karnataka, 570 020, India.
Eur J Nutr. 2017 Dec;56(8):2475-2485. doi: 10.1007/s00394-016-1283-0. Epub 2016 Aug 3.
Lutein's role on chronic hyperglycemia-induced oxidative stress and associated glucose homeostasis in heart and kidney is limited. Purpose of the study is to investigate the effect of lutein on cardiac and renal polyol pathway enzymes and oxidative stress markers under hyperglycemia-induced oxidative stress condition using streptozotocin (STZ)-injected rat model.
STZ-induced hyperglycemic (fasting blood glucose ≥11 mM) male Wistar rats were divided into two groups (n = 11/group). Group 1 received micellar lutein (39 nmol/day/rat) and group 2 (negative control) received micelle without lutein for 8 weeks. A separate group (no STZ injected) served as a positive control (n = 11/group). Oral glucose tolerance test (OGTT), biweekly urine glucose and activities of aldose reductase (AR) and sorbitol dehydrogenase (SDH) enzymes were assessed. Activities of antioxidant enzymes and antioxidant level were also evaluated.
Lutein-administered hyperglycemic rats showed better glucose tolerance as evidenced with OGTT and biweekly urine glucose when compared to negative control. Activities of AR and SDH were decreased in heart and kidney of lutein-fed hyperglycemic rats. Also, they had significantly (p < 0.05) decreased malondialdehyde levels (66, 34, and 33 %) and increased reduced glutathione level (81, 18 and 92 %) in serum, heart and kidney, respectively. Altered antioxidant enzyme activities such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione transferase were also affected in serum, heart and kidney of lutein-fed diabetic group.
Lutein prevented cardiac and renal injury in STZ-induced hyperglycemic rats due to potential amelioration of altered activities in polyol pathway and oxidative stress markers.
叶黄素在慢性高血糖诱导的氧化应激及相关葡萄糖稳态中的作用有限。本研究旨在通过链脲佐菌素(STZ)注射大鼠模型,研究叶黄素在高血糖诱导的氧化应激条件下对心脏和肾脏多元醇途径酶及氧化应激标志物的影响。
STZ 诱导的高血糖(空腹血糖≥11mmol/L)雄性 Wistar 大鼠分为两组(n=11/组)。第 1 组给予胶束叶黄素(39nmol/天/只),第 2 组(阴性对照)给予不含叶黄素的胶束,共 8 周。另设一组(未注射 STZ)作为阳性对照(n=11/组)。每周两次检测尿糖,并进行口服葡萄糖耐量试验(OGTT)。还评估了抗氧化酶的活性和抗氧化水平。
与阴性对照组相比,给予叶黄素的高血糖大鼠在 OGTT 和每周两次的尿糖检测中表现出更好的葡萄糖耐量。叶黄素喂养的高血糖大鼠心脏和肾脏中的醛糖还原酶(AR)和山梨醇脱氢酶(SDH)活性降低。此外,它们的血清、心脏和肾脏中的丙二醛水平分别降低了 66%、34%和 33%(p<0.05),还原型谷胱甘肽水平分别增加了 81%、18%和 92%。血清、心脏和肾脏中抗氧化酶活性如超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽转移酶也发生了改变。
叶黄素通过潜在改善多元醇途径和氧化应激标志物的活性,防止了 STZ 诱导的高血糖大鼠的心脏和肾脏损伤。