TITLE:
Garlic (allium sativum) modulates the expression of angiotensin II AT2 receptor in adrenal and renal tissues of streptozotocin-induced diabetic rats
AUTHORS:
Mohamed H. Mansour, Khaled Al-Qattan, Martha Thomson, Muslim Ali
KEYWORDS:
AT2 Receptor; Garlic; Streptozotocin-Induced Diabetes; Immunohistochemistry.
JOURNAL NAME:
Advances in Biological Chemistry,
Vol.1 No.3,
November
7,
2011
ABSTRACT: The loss of balance between the antagonistic activities of angiotensin II AT1/AT2 receptors has been impli-cated as a major mediator in the development of hypertension and progressive nephropathy in expe-rimental diabetes. The present study was designed to investigate the potential of garlic to modulate the level of expression of the AT2 receptor in the adrenal and renal tissues of diabetic rats. Three groups of rats were studied after 8 weeks following diabetes induction: normal, streptozotocin-induced diabetic (control diabetic), and garlic-treated diabetic rats. A polyclonal antibody of proven specificity to the AT2 receptor, as verified by Western blotting and emplo- yed in immunohistochemical assays, indicated that compared to normal rats, the highest adrenocortical AT2 receptor expression was significantly shifted from the zona glomerulosa to the zona fasciculate/ reticularis, and was significantly reduced in adrenomedul- lary chromaffin cells of control diabetic rats. In the kidney, STZ treatments were associated with a signi- ficant decrease in AT2 receptor expression throughout glomeruli and all cortical and medullary tubular segments. Compared to control diabetic rats, the labeling of the AT2 receptor in the garlic-treated diabetic group was restored among adrenocortical zona glomerulosa cells and adrenomedullary chromaffin cells and significantly reduced in the zona fasiculata, and was also restored in glomeruli and throughout renal cortical and medullary tubular segments, to le- vels comparable to those observed in normal rats. The capacity of garlic to modulate diabetes-induced AT2 receptor down-regulation may be implicated in restoring the recuperative processes mediated by AT2 receptors, which interfere with the development of hypertension and nephropathy.