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Astaxanthin Ameliorates Diabetic Retinopathy in Swiss Albino Mice via Inhibitory Processes of Neuron-Specific Enolase Activity
Retinopathy is one of the most common complications of diabetes mellitus. Diabetic retinopathy (DR) occurs due to microvascular damage in retinal tissues provoked by high blood sugar levels. The available drugs for DR are limited. Astaxanthin (AST) has anti-hypertensive, anti-obesity, and anti-diabe...
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Published in: | Processes 2022-07, Vol.10 (7), p.1318 |
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description | Retinopathy is one of the most common complications of diabetes mellitus. Diabetic retinopathy (DR) occurs due to microvascular damage in retinal tissues provoked by high blood sugar levels. The available drugs for DR are limited. Astaxanthin (AST) has anti-hypertensive, anti-obesity, and anti-diabetic properties. However, the therapeutic effect of AST on DR remains elusive. The present study is designed to investigate the effects of AST on DR via inhibition of neuron-specific enolase (NSE) activity. DR was induced by the administration of streptozotocin (STZ, 35 mg/kg: intraperitoneal; and 20 μL of STZ: intravitreal) in mice. AST (10 and 20 mg/kg) was administered orally (p.o.) for 21 days. The DR associated visual changes were assessed at different time intervals via optokinetic motor response (OMR) and penta-maze (PM) tests. Blood glucose level as well as retinal catalase, lactate dehydrogenase (LDH), & neuron-specific enolase (NSE) were estimated. The reference drug i.e., dexamethasone (DEX, 10 mg/kg; p.o.) was administered for 21 days. The administration of AST showed significant ameliorative potential in DR. Hence, AST can be used as a natural medicine for the management of DR due to its potential antioxidant, anti-diabetic, and NSE inhibitory properties. |
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Diabetic retinopathy (DR) occurs due to microvascular damage in retinal tissues provoked by high blood sugar levels. The available drugs for DR are limited. Astaxanthin (AST) has anti-hypertensive, anti-obesity, and anti-diabetic properties. However, the therapeutic effect of AST on DR remains elusive. The present study is designed to investigate the effects of AST on DR via inhibition of neuron-specific enolase (NSE) activity. DR was induced by the administration of streptozotocin (STZ, 35 mg/kg: intraperitoneal; and 20 μL of STZ: intravitreal) in mice. AST (10 and 20 mg/kg) was administered orally (p.o.) for 21 days. The DR associated visual changes were assessed at different time intervals via optokinetic motor response (OMR) and penta-maze (PM) tests. Blood glucose level as well as retinal catalase, lactate dehydrogenase (LDH), & neuron-specific enolase (NSE) were estimated. The reference drug i.e., dexamethasone (DEX, 10 mg/kg; p.o.) was administered for 21 days. 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This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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Diabetic retinopathy (DR) occurs due to microvascular damage in retinal tissues provoked by high blood sugar levels. The available drugs for DR are limited. Astaxanthin (AST) has anti-hypertensive, anti-obesity, and anti-diabetic properties. However, the therapeutic effect of AST on DR remains elusive. The present study is designed to investigate the effects of AST on DR via inhibition of neuron-specific enolase (NSE) activity. DR was induced by the administration of streptozotocin (STZ, 35 mg/kg: intraperitoneal; and 20 μL of STZ: intravitreal) in mice. AST (10 and 20 mg/kg) was administered orally (p.o.) for 21 days. The DR associated visual changes were assessed at different time intervals via optokinetic motor response (OMR) and penta-maze (PM) tests. Blood glucose level as well as retinal catalase, lactate dehydrogenase (LDH), & neuron-specific enolase (NSE) were estimated. The reference drug i.e., dexamethasone (DEX, 10 mg/kg; p.o.) was administered for 21 days. 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Thirunavukkarasu, Jayaraman ; Muthuraman, Arunachalam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c295t-28a473ca2458541f3b4512f09949b90a0db1223efe0948d419d9264cc8f872d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Albinism</topic><topic>Angiogenesis</topic><topic>Animals</topic><topic>Antihypertensives</topic><topic>Antioxidants</topic><topic>Astaxanthin</topic><topic>Blood</topic><topic>Catalase</topic><topic>Dexamethasone</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic retinopathy</topic><topic>Edema</topic><topic>Enzymes</topic><topic>Glucose</topic><topic>Hyperglycemia</topic><topic>L-Lactate dehydrogenase</topic><topic>Lactate dehydrogenase</topic><topic>Lactic acid</topic><topic>Metabolism</topic><topic>Microvasculature</topic><topic>Opto-kinetics</topic><topic>Oral administration</topic><topic>Phosphopyruvate hydratase</topic><topic>Proteins</topic><topic>Retina</topic><topic>Retinopathy</topic><topic>Streptozocin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Subramanian, Aswinprakash</creatorcontrib><creatorcontrib>Thirunavukkarasu, Jayaraman</creatorcontrib><creatorcontrib>Muthuraman, Arunachalam</creatorcontrib><collection>CrossRef</collection><collection>Engineered Materials Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Materials Research Database</collection><collection>https://resources.nclive.org/materials</collection><collection>ProQuest Biological Science Collection</collection><collection>ProQuest Biological Science Journals</collection><collection>Materials science collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Processes</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Subramanian, Aswinprakash</au><au>Thirunavukkarasu, Jayaraman</au><au>Muthuraman, Arunachalam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astaxanthin Ameliorates Diabetic Retinopathy in Swiss Albino Mice via Inhibitory Processes of Neuron-Specific Enolase Activity</atitle><jtitle>Processes</jtitle><date>2022-07-01</date><risdate>2022</risdate><volume>10</volume><issue>7</issue><spage>1318</spage><pages>1318-</pages><issn>2227-9717</issn><eissn>2227-9717</eissn><abstract>Retinopathy is one of the most common complications of diabetes mellitus. Diabetic retinopathy (DR) occurs due to microvascular damage in retinal tissues provoked by high blood sugar levels. The available drugs for DR are limited. Astaxanthin (AST) has anti-hypertensive, anti-obesity, and anti-diabetic properties. However, the therapeutic effect of AST on DR remains elusive. The present study is designed to investigate the effects of AST on DR via inhibition of neuron-specific enolase (NSE) activity. DR was induced by the administration of streptozotocin (STZ, 35 mg/kg: intraperitoneal; and 20 μL of STZ: intravitreal) in mice. AST (10 and 20 mg/kg) was administered orally (p.o.) for 21 days. The DR associated visual changes were assessed at different time intervals via optokinetic motor response (OMR) and penta-maze (PM) tests. Blood glucose level as well as retinal catalase, lactate dehydrogenase (LDH), & neuron-specific enolase (NSE) were estimated. The reference drug i.e., dexamethasone (DEX, 10 mg/kg; p.o.) was administered for 21 days. 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subjects | Albinism Angiogenesis Animals Antihypertensives Antioxidants Astaxanthin Blood Catalase Dexamethasone Diabetes Diabetes mellitus Diabetic retinopathy Edema Enzymes Glucose Hyperglycemia L-Lactate dehydrogenase Lactate dehydrogenase Lactic acid Metabolism Microvasculature Opto-kinetics Oral administration Phosphopyruvate hydratase Proteins Retina Retinopathy Streptozocin |
title | Astaxanthin Ameliorates Diabetic Retinopathy in Swiss Albino Mice via Inhibitory Processes of Neuron-Specific Enolase Activity |
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