Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar 608 002, Tamil Nadu, India.
Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar 608 002, Tamil Nadu, India.
Toxicol Appl Pharmacol. 2014 Sep 1;279(2):173-85. doi: 10.1016/j.taap.2014.05.014. Epub 2014 Jun 9.
Diabetic nephropathy is the kidney disease that occurs as a result of diabetes. The present study was aimed to evaluate the therapeutic potential of myricetin by assaying the activities of key enzymes of carbohydrate metabolism, insulin signaling molecules and renal function markers in streptozotocin (STZ)-cadmium (Cd) induced diabetic nephrotoxic rats. After myricetin treatment schedule, blood and tissue samples were collected to determine plasma glucose, insulin, hemoglobin, glycosylated hemoglobin and renal function markers, carbohydrate metabolic enzymes in the liver and insulin signaling molecules in the pancreas and skeletal muscle. A significant increase of plasma glucose, glycosylated hemoglobin, urea, uric acid, creatinine, blood urea nitrogen (BUN), urinary albumin, glycogen phosphorylase, glucose-6-phosphatase, and fructose-1,6-bisphosphatase and a significant decrease of plasma insulin, hemoglobin, hexokinase, glucose-6-phosphate dehydrogenase, glycogen and glycogen synthase with insulin signaling molecule expression were found in the STZ-Cd induced diabetic nephrotoxic rats. The administration of myricetin significantly normalizes the carbohydrate metabolic products like glucose, glycated hemoglobin, glycogen phosphorylase and gluconeogenic enzymes and renal function markers with increase insulin, glycogen, glycogen synthase and insulin signaling molecule expression like glucose transporter-2 (GLUT-2), glucose transporter-4 (GLUT-4), insulin receptor-1 (IRS-1), insulin receptor-2 (IRS-2) and protein kinase B (PKB). Based on the data, the protective effect of myricetin was confirmed by its histological annotation of the pancreas, liver and kidney tissues. These findings suggest that myricetin improved carbohydrate metabolism which subsequently enhances glucose utilization and renal function in STZ-Cd induced diabetic nephrotoxic rats.
糖尿病肾病是一种由于糖尿病而引起的肾脏疾病。本研究旨在通过测定链脲佐菌素（STZ）-镉（Cd）诱导的糖尿病肾病大鼠糖代谢关键酶、胰岛素信号分子和肾功能标志物的活性，评估杨梅素的治疗潜力。在杨梅素治疗方案结束后，收集血液和组织样本，以确定血浆葡萄糖、胰岛素、血红蛋白、糖化血红蛋白和肾功能标志物、肝脏糖代谢酶以及胰腺和骨骼肌中的胰岛素信号分子。STZ-Cd 诱导的糖尿病肾病大鼠的血浆葡萄糖、糖化血红蛋白、尿素、尿酸、肌酐、血尿素氮（BUN）、尿白蛋白、糖原磷酸化酶、葡萄糖-6-磷酸酶和果糖-1,6-二磷酸酶显著升高，而血浆胰岛素、血红蛋白、己糖激酶、葡萄糖-6-磷酸脱氢酶、糖原和糖原合酶以及胰岛素信号分子表达显著降低。杨梅素的给药显著使葡萄糖、糖化血红蛋白、糖原磷酸化酶和糖异生酶等糖代谢产物以及胰岛素、糖原、糖原合酶和胰岛素信号分子（如葡萄糖转运蛋白-2（GLUT-2）、葡萄糖转运蛋白-4（GLUT-4）、胰岛素受体-1（IRS-1）、胰岛素受体-2（IRS-2）和蛋白激酶 B（PKB））的表达恢复正常。基于这些数据，杨梅素对胰腺、肝脏和肾脏组织的组织学注释证实了其保护作用。这些发现表明，杨梅素改善了糖代谢，从而增强了 STZ-Cd 诱导的糖尿病肾病大鼠的葡萄糖利用和肾功能。
