Abstract
The ethanol extract from the rhizome of Zingiber zerumbet (L.) Smith (EEZZR) has been indicated to possess an insulin-like property by ameliorating hyperglycemia in diabetes. We aimed to investigate whether EEZZR exerts an ameliorative effect on renal damage in diabetes induced by streptozotocin (STZ). Diabetic rats were treated orally with EEZZR (200 and 300 mg kg−1 per day) or metformin (100 mg kg−1 per day) for 8 weeks. The plasma glucose, creatinine, and blood urea nitrogen as well as urine protein levels and the ratio of kidney weight to body weight were significantly elevated in diabetic rats. EEZZR displayed similar characteristics to those of metformin in reducing hyperglycemia and renal dysfunction in diabetic rats. The histological examinations revealed amelioration of diabetes-induced glomerular pathological changes following the treatment with EEZZR. In addition, the protein expressions of renal nephrin and podocin in diabetic rats were significantly increased following the treatment with EEZZR. The AMP-activated protein kinase (AMPK) protein phosphorylation and expression levels were remarkably reduced in diabetic renal tissues. EEZZR treatment significantly rescued the AMPK phosphorylation compared to nontreated diabetic group. This study suggested that the renoprotective effects of EEZZR may be similar, with the action of metformin, to the prevention of AMPK dephosphorylation and upregulate the expressions of renal nephrin and podocin.
Highlights
Hyperglycemia and several other symptoms are involved in the development of complications associated with diabetes
A significant increase in fasting blood glucose in STZ-diabetic rats was observed when compared to normal control group and this change was more marked at the 8th week following diabetes induction
The blood glucose lowering effect was obvious when STZ-diabetic rats were treated with 300 mg kg−1 EEZZR (28.1 ± 2.3%) and metformin (38.6 ± 4.3%) for 8 weeks (Table 1)
Summary
Hyperglycemia and several other symptoms are involved in the development of complications associated with diabetes. The glomerular vasculature consists of three structures that act in concert to prevent the development of albuminuria and proteinuria. These structures are the fenestrated endothelium, the glomerular basement membrane, and the epithelial slit diaphragm [3]. Hyperglycemia leads to a downregulation of negatively charged proteoglycans in the basement membrane of the glomerulus that has been demonstrated [4]. A role of the slit membrane in the pathogenesis of diabetic albuminuria has been suggested [5]. Amelioration of renal injury resulting in proteinuria in diabetes is reportedly associated with modulating the loss of glomerular permselectivity [6]
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