Abstract
Diabetes mellitus gradually leads to dysfunction and failure of some vital organs specially the eyes, kidneys, pancreas, brain, heart, liver and lungs. The study was aimed to evaluate the antidiabetic potential of apigenin and its mechanistic role in controlling damages of vital tissues in streptozotocin-induced diabetic rats. Streptozotocin-induced diabetic rats were treated with apigenin and glipizide. Various biochemical changes, GLUT4 and CD38 protein expression patterns and histopathological alterations in some vital organs such as liver, kidneys and pancreas were investigated to compare the antidiabetic potentials of those two chemicals and to understand their capability to control the damages of the vital organs during diabetes. Effective control of blood glucose level along with the alteration of hepatic phase I and phase II drug metabolizing enzymes, antioxidant defense enzyme activities and lipid peroxidation level towards their normal values and enhanced GLUT4 translocation and downregulated CD38 expression by apigenin were observed. Apigenin was also found to prevent the deterioration of vital organs during diabetes. In conclusion, apigenin has predominant role in controlling blood glucose level along with the protection of vital organs eventually damaged during diabetes, by minimizing toxicities and associated diabetic complications in streptozotocin-induced diabetic rats and may explore as a potential antidiabetic agent in near future.
Highlights
Injection for its treatment, whereas the cause of NIDDM is insulin resistance and NIDDM is managed by the
GLUT4 and Cluster of Differentiation 38 (CD38) protein expression patterns and histopathological alterations in some vital organs such as liver, kidneys and pancreas were investigated to compare the antidiabetic potentials of those two chemicals and to understand their capability to control the damages of the vital organs during diabetes
On day 14 after administration of STZ, all the rats belonging to group II, group III and group VI had significantly (p
Summary
Injection for its treatment, whereas the cause of NIDDM is insulin resistance and NIDDM is managed by the. Develop type 2 DM in animal model (King, 2012) It is IDDM is an autoimmune disease with complete reported that low dose STZ has been found to develop destruction of pancreatic β-cells and requires insulin type 2 DM in rats (Wilson and Islam, 2012). 4,5,7-trihydroxyflavone is a non-mutagenic flavone of a subclass of flavonoids with a very little toxicity (Cao et al, 2013) This compound has been reported to have anti-inflammatory, antioxidant and anti-carcinogenic properties (Liu et al, 2011). Effect of apigenin on STZ-induced diabetes in rats, histopathological alterations of different vital tissues such as liver, kidneys and pancreas, various biochemical alterations such as lipid peroxidation level, Phase I and phase II drug metabolizing enzymes, antioxidant defense enzymes and GLUT4 and CD38 protein expressions were investigated
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