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Metformin attenuated histopathological ocular deteriorations in a streptozotocin-induced hyperglycemic rat model
Diabetes mellitus (DM) often causes ocular disorders leading to vision loss. Metformin is commonly prescribed for type 2 diabetes. This study assessed the effect of metformin on hyperglycemic histopathological eye abnormalities and some possible pathways involved. Male rats were divided into 3 group...
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Published in: | Naunyn-Schmiedeberg's archives of pharmacology 2021-03, Vol.394 (3), p.457-467 |
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description | Diabetes mellitus (DM) often causes ocular disorders leading to vision loss. Metformin is commonly prescribed for type 2 diabetes. This study assessed the effect of metformin on hyperglycemic histopathological eye abnormalities and some possible pathways involved. Male rats were divided into 3 groups (
N
= 6), namely, healthy control, hyperglycemic non-treated control, and hyperglycemic rats treated with 200 mg/kg metformin. Two weeks after diabetes induction by an intraperitoneal streptozotocin (60 mg streptozotocin (STZ)/kg) injection, the rats develop ocular abnormalities, and metformin (200 mg/kg) treatment was administered daily. Rats underwent dilated retinal digital ophthalmoscope examination and graded for diabetic retinopathy. Rats were sacrificed at 12 weeks, and the cornea, lens, sclera, ciliary body, iris, conjunctiva, retinal, and optic nerve were examined histologically. Rats’ fasting blood glucose and body weight were monitored. Serum tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), claudin-1, and glutathione/malondialdehyde ratios were analyzed. Metformin significantly attenuated diabetes-related histopathological ocular deteriorations in the cornea, lens, sclera, ciliary body, iris, conjunctiva, retina, and optic nerve partly by restoring serum TNF-α, VEGF, claudin-1, and glutathione/malondialdehyde ratios without significantly affecting the fasting blood glucose levels or body weight in these hyperglycemic rats. Metformin attenuated hyperglycemia-associated histopathological eye deteriorations, possibly partly by ameliorating vascular leakage, oxidative stress, inflammation, and neovascularization, without affecting the fasting blood glucose levels or body weights in these STZ-induced diabetic rats. |
doi_str_mv | 10.1007/s00210-020-01989-w |
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N
= 6), namely, healthy control, hyperglycemic non-treated control, and hyperglycemic rats treated with 200 mg/kg metformin. Two weeks after diabetes induction by an intraperitoneal streptozotocin (60 mg streptozotocin (STZ)/kg) injection, the rats develop ocular abnormalities, and metformin (200 mg/kg) treatment was administered daily. Rats underwent dilated retinal digital ophthalmoscope examination and graded for diabetic retinopathy. Rats were sacrificed at 12 weeks, and the cornea, lens, sclera, ciliary body, iris, conjunctiva, retinal, and optic nerve were examined histologically. Rats’ fasting blood glucose and body weight were monitored. Serum tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), claudin-1, and glutathione/malondialdehyde ratios were analyzed. Metformin significantly attenuated diabetes-related histopathological ocular deteriorations in the cornea, lens, sclera, ciliary body, iris, conjunctiva, retina, and optic nerve partly by restoring serum TNF-α, VEGF, claudin-1, and glutathione/malondialdehyde ratios without significantly affecting the fasting blood glucose levels or body weight in these hyperglycemic rats. Metformin attenuated hyperglycemia-associated histopathological eye deteriorations, possibly partly by ameliorating vascular leakage, oxidative stress, inflammation, and neovascularization, without affecting the fasting blood glucose levels or body weights in these STZ-induced diabetic rats.</description><identifier>ISSN: 0028-1298</identifier><identifier>EISSN: 1432-1912</identifier><identifier>DOI: 10.1007/s00210-020-01989-w</identifier><identifier>PMID: 33047165</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Antidiabetics ; Biomedical and Life Sciences ; Biomedicine ; Blood glucose ; Body weight ; Claudin-1 - blood ; Conjunctiva ; Cornea ; Diabetes ; Diabetes Complications - blood ; Diabetes Complications - drug therapy ; Diabetes Complications - pathology ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - pathology ; Diabetic retinopathy ; Eye Diseases - blood ; Eye Diseases - drug therapy ; Eye Diseases - etiology ; Eye Diseases - pathology ; Eye disorders ; Fasting ; Glucose ; Glutathione ; Glutathione - blood ; Hyperglycemia ; Hyperglycemia - blood ; Hyperglycemia - chemically induced ; Hyperglycemia - drug therapy ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Inflammation ; Iris ; Male ; Malondialdehyde ; Malondialdehyde - blood ; Metformin ; Metformin - pharmacology ; Metformin - therapeutic use ; Neurosciences ; Optic nerve ; Original Article ; Oxidative stress ; Pharmacology/Toxicology ; Rats ; Rats, Sprague-Dawley ; Retina ; Retinopathy ; Rodents ; Streptozocin ; Tumor Necrosis Factor-alpha - blood ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - blood ; Vascularization</subject><ispartof>Naunyn-Schmiedeberg's archives of pharmacology, 2021-03, Vol.394 (3), p.457-467</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020</rights><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-5c22a55275fa3abde0c259ebcf7d406712016b479d51ea413f79c1f8dce55cad3</citedby><cites>FETCH-LOGICAL-c441t-5c22a55275fa3abde0c259ebcf7d406712016b479d51ea413f79c1f8dce55cad3</cites><orcidid>0000-0002-2954-3821</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33047165$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nahar, Nazmun</creatorcontrib><creatorcontrib>Mohamed, Suhaila</creatorcontrib><creatorcontrib>Mustapha, Noordin Mohamed</creatorcontrib><creatorcontrib>Lau, SengFong</creatorcontrib><creatorcontrib>Ishak, Nur Iliyani Mohd</creatorcontrib><creatorcontrib>Umran, Norshahira Solehah</creatorcontrib><title>Metformin attenuated histopathological ocular deteriorations in a streptozotocin-induced hyperglycemic rat model</title><title>Naunyn-Schmiedeberg's archives of pharmacology</title><addtitle>Naunyn-Schmiedeberg's Arch Pharmacol</addtitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><description>Diabetes mellitus (DM) often causes ocular disorders leading to vision loss. Metformin is commonly prescribed for type 2 diabetes. This study assessed the effect of metformin on hyperglycemic histopathological eye abnormalities and some possible pathways involved. Male rats were divided into 3 groups (
N
= 6), namely, healthy control, hyperglycemic non-treated control, and hyperglycemic rats treated with 200 mg/kg metformin. Two weeks after diabetes induction by an intraperitoneal streptozotocin (60 mg streptozotocin (STZ)/kg) injection, the rats develop ocular abnormalities, and metformin (200 mg/kg) treatment was administered daily. Rats underwent dilated retinal digital ophthalmoscope examination and graded for diabetic retinopathy. Rats were sacrificed at 12 weeks, and the cornea, lens, sclera, ciliary body, iris, conjunctiva, retinal, and optic nerve were examined histologically. Rats’ fasting blood glucose and body weight were monitored. Serum tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), claudin-1, and glutathione/malondialdehyde ratios were analyzed. Metformin significantly attenuated diabetes-related histopathological ocular deteriorations in the cornea, lens, sclera, ciliary body, iris, conjunctiva, retina, and optic nerve partly by restoring serum TNF-α, VEGF, claudin-1, and glutathione/malondialdehyde ratios without significantly affecting the fasting blood glucose levels or body weight in these hyperglycemic rats. Metformin attenuated hyperglycemia-associated histopathological eye deteriorations, possibly partly by ameliorating vascular leakage, oxidative stress, inflammation, and neovascularization, without affecting the fasting blood glucose levels or body weights in these STZ-induced diabetic rats.</description><subject>Animals</subject><subject>Antidiabetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood glucose</subject><subject>Body weight</subject><subject>Claudin-1 - blood</subject><subject>Conjunctiva</subject><subject>Cornea</subject><subject>Diabetes</subject><subject>Diabetes Complications - blood</subject><subject>Diabetes Complications - drug therapy</subject><subject>Diabetes Complications - pathology</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetic retinopathy</subject><subject>Eye Diseases - blood</subject><subject>Eye Diseases - drug therapy</subject><subject>Eye Diseases - etiology</subject><subject>Eye Diseases - pathology</subject><subject>Eye disorders</subject><subject>Fasting</subject><subject>Glucose</subject><subject>Glutathione</subject><subject>Glutathione - blood</subject><subject>Hyperglycemia</subject><subject>Hyperglycemia - blood</subject><subject>Hyperglycemia - chemically induced</subject><subject>Hyperglycemia - drug therapy</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Inflammation</subject><subject>Iris</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - blood</subject><subject>Metformin</subject><subject>Metformin - pharmacology</subject><subject>Metformin - therapeutic use</subject><subject>Neurosciences</subject><subject>Optic nerve</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Retina</subject><subject>Retinopathy</subject><subject>Rodents</subject><subject>Streptozocin</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - blood</subject><subject>Vascularization</subject><issn>0028-1298</issn><issn>1432-1912</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kcFO3DAURS1EBQPtD7CoInXTTYqfY8fxskJtQaJiU9aWx34ZjJI42I7Q9OvrYaBILFhYXrxzj598CTkD-g0oleeJUga0pqwcUJ2qHw_ICnjDalDADsmqzLsamOqOyUlK95TSFoQ4IsdNQ7mEVqzI_BtzH-Lop8rkjNNiMrrqzqccZpPvwhA23pqhCnYZTKwcZow-RJN9mFK1S1UpR5xz-BtysH6q_eQWu3NsZ4ybYWtx9LYqiWoMDoeP5ENvhoSfnu9Tcvvzx5-Ly_r65tfVxffr2nIOuRaWMSMEk6I3jVk7pJYJhWvbS8dpK4FRaNdcKicADYeml8pC3zmLQljjmlPyde-dY3hYMGU9-mRxGMyEYUmacVE05YdkQb-8Qe_DEqeyXaEU7TqpWl4otqdsDClF7PUc_WjiVgPVuz70vg9d-tBPfejHEvr8rF7WI7r_kZcCCtDsgVRG0wbj69vvaP8BX_uZQg</recordid><startdate>20210301</startdate><enddate>20210301</enddate><creator>Nahar, Nazmun</creator><creator>Mohamed, Suhaila</creator><creator>Mustapha, Noordin Mohamed</creator><creator>Lau, SengFong</creator><creator>Ishak, Nur Iliyani Mohd</creator><creator>Umran, Norshahira Solehah</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2954-3821</orcidid></search><sort><creationdate>20210301</creationdate><title>Metformin attenuated histopathological ocular deteriorations in a streptozotocin-induced hyperglycemic rat model</title><author>Nahar, Nazmun ; Mohamed, Suhaila ; Mustapha, Noordin Mohamed ; Lau, SengFong ; Ishak, Nur Iliyani Mohd ; Umran, Norshahira Solehah</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-5c22a55275fa3abde0c259ebcf7d406712016b479d51ea413f79c1f8dce55cad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Antidiabetics</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood glucose</topic><topic>Body weight</topic><topic>Claudin-1 - blood</topic><topic>Conjunctiva</topic><topic>Cornea</topic><topic>Diabetes</topic><topic>Diabetes Complications - blood</topic><topic>Diabetes Complications - drug therapy</topic><topic>Diabetes Complications - pathology</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetic retinopathy</topic><topic>Eye Diseases - blood</topic><topic>Eye Diseases - drug therapy</topic><topic>Eye Diseases - etiology</topic><topic>Eye Diseases - pathology</topic><topic>Eye disorders</topic><topic>Fasting</topic><topic>Glucose</topic><topic>Glutathione</topic><topic>Glutathione - blood</topic><topic>Hyperglycemia</topic><topic>Hyperglycemia - blood</topic><topic>Hyperglycemia - chemically induced</topic><topic>Hyperglycemia - drug therapy</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Inflammation</topic><topic>Iris</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - blood</topic><topic>Metformin</topic><topic>Metformin - pharmacology</topic><topic>Metformin - therapeutic use</topic><topic>Neurosciences</topic><topic>Optic nerve</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Pharmacology/Toxicology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Retina</topic><topic>Retinopathy</topic><topic>Rodents</topic><topic>Streptozocin</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - blood</topic><topic>Vascularization</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nahar, Nazmun</creatorcontrib><creatorcontrib>Mohamed, Suhaila</creatorcontrib><creatorcontrib>Mustapha, Noordin Mohamed</creatorcontrib><creatorcontrib>Lau, SengFong</creatorcontrib><creatorcontrib>Ishak, Nur Iliyani Mohd</creatorcontrib><creatorcontrib>Umran, Norshahira Solehah</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest - 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Academic</collection><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nahar, Nazmun</au><au>Mohamed, Suhaila</au><au>Mustapha, Noordin Mohamed</au><au>Lau, SengFong</au><au>Ishak, Nur Iliyani Mohd</au><au>Umran, Norshahira Solehah</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metformin attenuated histopathological ocular deteriorations in a streptozotocin-induced hyperglycemic rat model</atitle><jtitle>Naunyn-Schmiedeberg's archives of pharmacology</jtitle><stitle>Naunyn-Schmiedeberg's Arch Pharmacol</stitle><addtitle>Naunyn Schmiedebergs Arch Pharmacol</addtitle><date>2021-03-01</date><risdate>2021</risdate><volume>394</volume><issue>3</issue><spage>457</spage><epage>467</epage><pages>457-467</pages><issn>0028-1298</issn><eissn>1432-1912</eissn><abstract>Diabetes mellitus (DM) often causes ocular disorders leading to vision loss. Metformin is commonly prescribed for type 2 diabetes. This study assessed the effect of metformin on hyperglycemic histopathological eye abnormalities and some possible pathways involved. Male rats were divided into 3 groups (
N
= 6), namely, healthy control, hyperglycemic non-treated control, and hyperglycemic rats treated with 200 mg/kg metformin. Two weeks after diabetes induction by an intraperitoneal streptozotocin (60 mg streptozotocin (STZ)/kg) injection, the rats develop ocular abnormalities, and metformin (200 mg/kg) treatment was administered daily. Rats underwent dilated retinal digital ophthalmoscope examination and graded for diabetic retinopathy. Rats were sacrificed at 12 weeks, and the cornea, lens, sclera, ciliary body, iris, conjunctiva, retinal, and optic nerve were examined histologically. Rats’ fasting blood glucose and body weight were monitored. Serum tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), claudin-1, and glutathione/malondialdehyde ratios were analyzed. Metformin significantly attenuated diabetes-related histopathological ocular deteriorations in the cornea, lens, sclera, ciliary body, iris, conjunctiva, retina, and optic nerve partly by restoring serum TNF-α, VEGF, claudin-1, and glutathione/malondialdehyde ratios without significantly affecting the fasting blood glucose levels or body weight in these hyperglycemic rats. Metformin attenuated hyperglycemia-associated histopathological eye deteriorations, possibly partly by ameliorating vascular leakage, oxidative stress, inflammation, and neovascularization, without affecting the fasting blood glucose levels or body weights in these STZ-induced diabetic rats.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>33047165</pmid><doi>10.1007/s00210-020-01989-w</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-2954-3821</orcidid></addata></record> |
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subjects | Animals Antidiabetics Biomedical and Life Sciences Biomedicine Blood glucose Body weight Claudin-1 - blood Conjunctiva Cornea Diabetes Diabetes Complications - blood Diabetes Complications - drug therapy Diabetes Complications - pathology Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - pathology Diabetic retinopathy Eye Diseases - blood Eye Diseases - drug therapy Eye Diseases - etiology Eye Diseases - pathology Eye disorders Fasting Glucose Glutathione Glutathione - blood Hyperglycemia Hyperglycemia - blood Hyperglycemia - chemically induced Hyperglycemia - drug therapy Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Inflammation Iris Male Malondialdehyde Malondialdehyde - blood Metformin Metformin - pharmacology Metformin - therapeutic use Neurosciences Optic nerve Original Article Oxidative stress Pharmacology/Toxicology Rats Rats, Sprague-Dawley Retina Retinopathy Rodents Streptozocin Tumor Necrosis Factor-alpha - blood Tumor necrosis factor-TNF Tumor necrosis factor-α Vascular endothelial growth factor Vascular Endothelial Growth Factor A - blood Vascularization |
title | Metformin attenuated histopathological ocular deteriorations in a streptozotocin-induced hyperglycemic rat model |
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