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KMID : 1204320090250020139
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Laboratory Animal Research
2009 Volume.25 No. 2 p.139 ~ p.143
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Captopril Prevents the Activation of Mitogen Activated Protein Kinases, Akt, and NF-κB Signaling in Streptozotocin-induced Diabetic Retinopathy
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Han Ho-Jae
Park Soo-Hyun
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Abstract
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The retina is a very important organ in vision. Retinal dysfunction occurs in diabetic retinopathy, which is thought to be caused by an aberrant renin-angiotensin system (RAS). Angiotensin converting enzyme (ACE) is a key component of RAS. Diverse signaling molecules are involved in the development of diabetic retinopathy; mitogen activated protein kinases (MAPK) including p38 MAPK, p44/42 MAPK, and JNK 1/2 have been implicated in diabetes associated retinal dysfunction. Akt and nuclear factor-kappa B (NF-κB) also have roles in retinal function. The relationship between ACE and these signaling molecules in diabetic retinopathy is unclear. The present study investigated the protective effect of the ACE inhibitor captopril in the retina of streptozotocin (STZ)-induced diabetic rats. Increased phosphorylation of retinal p38 MAPK, p44/42 MAPK, JNK, Akt, and NF-κB in diabetic rats was uniformly blocked by captopril. The same retinas displayed decreased expression of mRNA for EAAC-1 and GLSAT-1, which was obviated by captopril. In conclusion, captopril prevented the expression of mitogen activated protein kinase, Akt, NF-κB signaling, and glutamate transpoter in the retina of STZ-induced diabetic rats.
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KEYWORD
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Angiotensin converting enzyme, mitogen activated protein kinase, Akt, NF-κB, diabetic retinopathy
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