Why the study?
Does telmisartan reduce oxidative stress and renal fibrosis in STZ-induced diabetic mice?
Does telmisartan reduce oxidative stress and renal fibrosis in STZ-induced diabetic mice?
Telmisartan attenuates oxidative stress and renal fibrosis in a mouse model of diabetic nephropathy, potentially through PPAR-γ agonist action and alteration of Ang-(1-7) mas receptor expression.
Should not yet change practice in diabetic nephropathy; leaves open whether molecular effects translate from mice to humans.
The beneficial effects of telmisartan on Angiotensin (Ang)-II mediated oxidative stress and renal fibrosis in streptozotocin (STZ)-induced diabetic nephropathy (DN) were studied. Thirty mice were divided into normal (NG), STZ-induced diabetic (DG) and telmisartan-treated diabetic (TG) groups. Compared with NG mice, DG mice showed significant up-regulations of AT-1R, TGF-β1, p-p38MAPK, p-MAPKAPK-2, p-Akt, p47phox, p67phox, gp91phox protein and collagen-III and all of these were significantly reversed in TG mice. The down-regulated protein expression of Ang-(1-7) mas receptor, ACE-2, PPAR-γ and PGC-1α were observed in DG mice and a significant up-regulation effect of telmisartan has been seen in the TG mice. Furthermore, TG mice showed reduced expression of fibronectin, production of superoxide radical as well as renal hypertrophy and fibrosis when compared with DG mice. These findings suggest that Ang-II plays a significant role in DN and telmisartan would be beneficial in reducing oxidative stress and fibrosis in STZ-induced DN.
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Lakshmanan et al. (2011) studied this question.
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