Telmisartan Ameliorates Neurotrophic Support and Oxidative Stress in the Retina of Streptozotocin-Induced Diabetic Rats
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ORIGINAL PAPER
Telmisartan Ameliorates Neurotrophic Support and Oxidative Stress in the Retina of Streptozotocin-Induced Diabetic Rats M. Shamsul Ola • Mohammed M. Ahmed • Hatem M. Abuohashish • Salim S. Al-Rejaie Abdullah S. Alhomida
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Received: 3 March 2013 / Revised: 17 April 2013 / Accepted: 19 April 2013 / Published online: 27 April 2013 Ó Springer Science+Business Media New York 2013
Abstract Neurodegeneration is an early event in the diabetic retina which may lead to diabetic retinopathy. One of the potential pathways in damaging retinal neurons is the activation of renin angiotensin system including angiotensin II type 1 receptor (AT1R) in the diabetic retina. The purpose of this study was to determine the effect of telmisartan, an AT1R blocker on retinal level of brain derived neurotrophic factor (BDNF), ciliary neurotrophic factor (CNTF) and tyrosine hydroxylase (TH), glutathione (GSH) and caspase activity in the diabetic rats. The dysregulated levels of these factors are known to cause neurodegeneration in diabetic retina. Three weeks streptozotocin induced diabetic rats were orally treated or untreated with telmisartan (10 mg/kg/day). After 4 weeks of treatments, the levels of BDNF and GSH were found to be increased systemically in the sera as well as in the retina of diabetic rats compared to untreated rats as measured by enzymelinked immunosorbent assay and biochemical techniques (p \ 0.05). The caspase-3 activity in the telmisartan treated diabetic retina was decreased compared to untreated diabetic rats (p \ 0.05). Western blotting experiments showed the expression levels of BDNF, CNTF and TH were increased compared to untreated diabetic rats (p \ 0.05). Thus, our findings show a beneficial effect of AT1R blocker telmisartan in efficiently increasing neurotrophic support, endogenous antioxidant GSH content, and decreasing signs of apoptosis in diabetic retina. M. S. Ola (&) A. S. Alhomida Department of Biochemistry, College of Science, King Saud University, Riyadh 11415, Saudi Arabia e-mail: [email protected]; [email protected] M. M. Ahmed H. M. Abuohashish S. S. Al-Rejaie Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia
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Keywords Diabetic retinopathy Telmisartan Neurodegeneration Brain derived neurotrophic factor Retina Apoptosis
Introduction Hypertension has been widely recognized as a potential risk factor for the damage of vasculature in several diabetic induced complications including retinopathy and nephropathy [1–4]. In diabetes, the components of renin angiotensin system (RAS) were found to be increased both systemically and locally in several tissues causing hypertension and the tissue damage. Recent studies in rodent’s model have revealed that components of RAS comprising of renin, prorenin, angiotensin II and its receptors are expressed in the retina and diabetes caused an increase in their expression [5, 6]. In addition, increased levels of the components of RAS were also observed in the vitreous of patien
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