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Iranian Journal of Pharmaceutical Research 2011

The Effects of Total Flavonoids from Buckwheat Flowers and Leaves on Renal Damage and PTP1B Expression in Type 2 Diabetic Rats.

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Jin-Xiu Chu
Zhi-Lu Wang
Shu-Ying Han

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Clinical data showed consumption of buckwheat played a very positive role in the relief of diabetes and its complications. The purpose of this study was to explore the effects and mechanisms of the overall flavonoids from buckwheat flowers and leaves (TFBFL) on renal damage in type 2 diabetes mellitus (T2DM) rats. Seventy male Wistar rats were selected. Ten rats were randomly allocated into a normal group and the other sixty were intragastrically injected with a lipid emulsion and small doses of alloxan to induce the T2DM model. T2DM inducement was judged by the fasting blood glucose (FBG) and oral glucose tolerance test (OGTT). Those whose FBG was ≥ 16.7 mmol/L and less tolerant to glucose were considered as being T2DM rats. These rats were then randomly divided into a groups termed: model (purified water, 5 mL.kg(-1) . d(-1)), BNPL (positive control) (Benazepril, 4 mg.kg(-1) . d(-1)), L-TFBFL (TFBFL 100 mg.kg(-1) . d(-1)), M-TFBFL (TBFL 200 mg.kg(-1) . d(-1)) and H-TFBFL (TFBFL 400 mg.kg(-1) . d(-1)). Each group then received medication for a period of 4 weeks. The normal rats were treated with purified water in a synchronous manner. Subsequently, FBG, plasma insulin (INS), OGTT, 24 h urinary protein output, blood and urinary creatinine content were assayed. Then the insulin sensitive index (ISI), bilateral kidney index, and creatinine clearance rate (Ccr) were calculated. Renal morphological changes and expression of protein tyrosine phosphatase 1B (PTP1B) in the kidneys were observed. TFBFL lowered FBG, improved insulin resistance, caused Ccr, and renal morphological changes, down-regulated the expression of PTP1B in T2DM rats and showed dose-dependence. TFBFL had a significant protective effect on renal damage in T2DM rats. This effect may be due to lowering blood glucose and diminishing renal damage by inhibiting PTP1B expression.

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