Novel antioxidant astaxanthin-s-allyl cysteine biconjugate diminished oxidative stress and mitochondrial dysfunction to triumph diabetes in rat model
The present study determines the effect of administration of novel antioxidant astaxanthin-s-allyl cysteine biconjugate (AST-SAC) against streptozotocin-induced diabetes mellitus (DM) in rats. AST-SAC (1 mg/kg/day) was treated against DM in rats for 45 days. The oxidative stress, antioxidants level,...
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| Veröffentlicht in: | Life sciences (1973) 2020-03, Vol.245, p.117367-11, Article 117367 |
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| creator | Penislusshiyan, Sakayanathan Chitra, Loganathan Ancy, Iruthayaraj Kumaradhas, Poomani Palvannan, Thayumanavan |
| description | The present study determines the effect of administration of novel antioxidant astaxanthin-s-allyl cysteine biconjugate (AST-SAC) against streptozotocin-induced diabetes mellitus (DM) in rats.
AST-SAC (1 mg/kg/day) was treated against DM in rats for 45 days. The oxidative stress, antioxidants level, insulin secretion, activities of various carbohydrate metabolizing enzymes were studied. The glucose uptake in L6 myotubes was studied. In addition, in silico analysis of interaction of AST-SAC with proteins such as insulin receptor (IR) and 5′-adenosine monophosphate-activated protein kinase (AMPK) were carried out.
Administration of AST-SAC in DM rats has protected the mitochondrial function (decreased oxidative stress and normalized oxidative phosphorylation activities) and antioxidant capacity of the pancreas which has resulted in beta cells rejuvenation and insulin secretion restoration. AST-SAC decreased the alpha-glucosidases activities to bring glycemic control in DM rats. Due to these effects the glycoprotein components and lipids were restored to near normalcy in DM rats. AST-SAC protected the antioxidant status of liver, kidney and plasma; and curbed the progression of secondary complications of DM. AST-SAC treatment stimulated glucose uptake in L6 myotubes in in vitro. To support this observation, AST-SAC interacted with proteins such as IR and AMPK in silico.
AST-SAC can be considered as “multi-target-directed ligand”, that is, through these manifold effects, AST-SAC has been able to prevail over DM in rats.
[Display omitted]
•Astaxanthin-s-allyl cysteine biconjugate (AST-SAC) eased diabetes mellitus (DM).•AST-SAC improved overall as well as mitochondrial antioxidant status against DM.•AST-SAC protected the mitochondrial function against DM.•AST-SAC reduced small intestinal α-glucosidases activities against DM.•AST-SAC simulated glucose uptake in skeletal muscle cells. |
| doi_str_mv | 10.1016/j.lfs.2020.117367 |
| format | Article |
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AST-SAC (1 mg/kg/day) was treated against DM in rats for 45 days. The oxidative stress, antioxidants level, insulin secretion, activities of various carbohydrate metabolizing enzymes were studied. The glucose uptake in L6 myotubes was studied. In addition, in silico analysis of interaction of AST-SAC with proteins such as insulin receptor (IR) and 5′-adenosine monophosphate-activated protein kinase (AMPK) were carried out.
Administration of AST-SAC in DM rats has protected the mitochondrial function (decreased oxidative stress and normalized oxidative phosphorylation activities) and antioxidant capacity of the pancreas which has resulted in beta cells rejuvenation and insulin secretion restoration. AST-SAC decreased the alpha-glucosidases activities to bring glycemic control in DM rats. Due to these effects the glycoprotein components and lipids were restored to near normalcy in DM rats. AST-SAC protected the antioxidant status of liver, kidney and plasma; and curbed the progression of secondary complications of DM. AST-SAC treatment stimulated glucose uptake in L6 myotubes in in vitro. To support this observation, AST-SAC interacted with proteins such as IR and AMPK in silico.
AST-SAC can be considered as “multi-target-directed ligand”, that is, through these manifold effects, AST-SAC has been able to prevail over DM in rats.
[Display omitted]
•Astaxanthin-s-allyl cysteine biconjugate (AST-SAC) eased diabetes mellitus (DM).•AST-SAC improved overall as well as mitochondrial antioxidant status against DM.•AST-SAC protected the mitochondrial function against DM.•AST-SAC reduced small intestinal α-glucosidases activities against DM.•AST-SAC simulated glucose uptake in skeletal muscle cells.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2020.117367</identifier><identifier>PMID: 32001265</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Adenosine kinase ; Adenosine monophosphate ; AMP ; Animals ; Antidiabetes ; Antioxidants ; Antioxidants - pharmacology ; Antioxidants - therapeutic use ; Astaxanthin ; Astaxanthin-s-allyl cysteine diester ; Beta cells ; Carbohydrates ; Cholesterol - metabolism ; Complications ; Cysteine ; Cysteine - analogs & derivatives ; Cysteine - pharmacology ; Cysteine - therapeutic use ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Glucose ; Glucose - metabolism ; Glycoproteins ; Hypoglycemic Agents - therapeutic use ; Insulin ; Insulin secretion ; Kidneys ; Kinases ; Lipids ; Male ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Molecular Docking Simulation ; Myotubes ; Oxidative phosphorylation ; Oxidative stress ; Oxidative Stress - drug effects ; Pancreas ; Phosphorylation ; Protein kinase ; Proteins ; Rats ; Rats, Sprague-Dawley ; Restoration ; Secretion ; Streptozocin ; Triglycerides - metabolism ; Xanthophylls - pharmacology ; Xanthophylls - therapeutic use</subject><ispartof>Life sciences (1973), 2020-03, Vol.245, p.117367-11, Article 117367</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Mar 15, 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-697b0991c71fcb54917c21c5d216bd31e42f13000c85aa63cd6b7840f5d8c67a3</citedby><cites>FETCH-LOGICAL-c381t-697b0991c71fcb54917c21c5d216bd31e42f13000c85aa63cd6b7840f5d8c67a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0024320520301144$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32001265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Penislusshiyan, Sakayanathan</creatorcontrib><creatorcontrib>Chitra, Loganathan</creatorcontrib><creatorcontrib>Ancy, Iruthayaraj</creatorcontrib><creatorcontrib>Kumaradhas, Poomani</creatorcontrib><creatorcontrib>Palvannan, Thayumanavan</creatorcontrib><title>Novel antioxidant astaxanthin-s-allyl cysteine biconjugate diminished oxidative stress and mitochondrial dysfunction to triumph diabetes in rat model</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>The present study determines the effect of administration of novel antioxidant astaxanthin-s-allyl cysteine biconjugate (AST-SAC) against streptozotocin-induced diabetes mellitus (DM) in rats.
AST-SAC (1 mg/kg/day) was treated against DM in rats for 45 days. The oxidative stress, antioxidants level, insulin secretion, activities of various carbohydrate metabolizing enzymes were studied. The glucose uptake in L6 myotubes was studied. In addition, in silico analysis of interaction of AST-SAC with proteins such as insulin receptor (IR) and 5′-adenosine monophosphate-activated protein kinase (AMPK) were carried out.
Administration of AST-SAC in DM rats has protected the mitochondrial function (decreased oxidative stress and normalized oxidative phosphorylation activities) and antioxidant capacity of the pancreas which has resulted in beta cells rejuvenation and insulin secretion restoration. AST-SAC decreased the alpha-glucosidases activities to bring glycemic control in DM rats. Due to these effects the glycoprotein components and lipids were restored to near normalcy in DM rats. AST-SAC protected the antioxidant status of liver, kidney and plasma; and curbed the progression of secondary complications of DM. AST-SAC treatment stimulated glucose uptake in L6 myotubes in in vitro. To support this observation, AST-SAC interacted with proteins such as IR and AMPK in silico.
AST-SAC can be considered as “multi-target-directed ligand”, that is, through these manifold effects, AST-SAC has been able to prevail over DM in rats.
[Display omitted]
•Astaxanthin-s-allyl cysteine biconjugate (AST-SAC) eased diabetes mellitus (DM).•AST-SAC improved overall as well as mitochondrial antioxidant status against DM.•AST-SAC protected the mitochondrial function against DM.•AST-SAC reduced small intestinal α-glucosidases activities against DM.•AST-SAC simulated glucose uptake in skeletal muscle cells.</description><subject>Adenosine kinase</subject><subject>Adenosine monophosphate</subject><subject>AMP</subject><subject>Animals</subject><subject>Antidiabetes</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Antioxidants - therapeutic use</subject><subject>Astaxanthin</subject><subject>Astaxanthin-s-allyl cysteine diester</subject><subject>Beta cells</subject><subject>Carbohydrates</subject><subject>Cholesterol - metabolism</subject><subject>Complications</subject><subject>Cysteine</subject><subject>Cysteine - analogs & derivatives</subject><subject>Cysteine - pharmacology</subject><subject>Cysteine - therapeutic use</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Glycoproteins</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin</subject><subject>Insulin secretion</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Male</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Molecular Docking Simulation</subject><subject>Myotubes</subject><subject>Oxidative phosphorylation</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pancreas</subject><subject>Phosphorylation</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Restoration</subject><subject>Secretion</subject><subject>Streptozocin</subject><subject>Triglycerides - metabolism</subject><subject>Xanthophylls - pharmacology</subject><subject>Xanthophylls - therapeutic use</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2OFCEUhYlx4rSjD-DGkLhxUy0_RVEVV2biXzKZ2eiaUHDLpkJBC1Rn-kHmfaXt0YUL2Vwg3zkX7kHoFSVbSmj3bt76KW8ZYfVMJe_kE7ShvRwa0nH6FG0IYW3DGRGX6HnOMyFECMmfoct6RyjrxAY93MYDeKxDcfHe2VqxzkXf183OhSY32vujx-aYC7gAeHQmhnn9oQtg6xYXXN6Bxb-1xR0A55Ig52po8eJKNLsYbHLaY3vM0xpM7RNwibgkty77XTXRIxTI2AWcdMFLtOBfoItJ-wwvH-sV-v7p47frL83N3eev1x9uGsN7WppukCMZBmokncwo2oFKw6gRltFutJxCyybK67dNL7TuuLHdKPuWTML2ppOaX6G3Z999ij9XyEUtLhvwXgeIa1aMC0KGOl9Z0Tf_oHNcU6ivU6zlgp3WUCl6pkyKOSeY1D65RaejokSdMlOzqpmpU2bqnFnVvH50XscF7F_Fn5Aq8P4MQB3FwUFS2TgIBqxLYIqy0f3H_hd9cKny</recordid><startdate>20200315</startdate><enddate>20200315</enddate><creator>Penislusshiyan, Sakayanathan</creator><creator>Chitra, Loganathan</creator><creator>Ancy, Iruthayaraj</creator><creator>Kumaradhas, Poomani</creator><creator>Palvannan, Thayumanavan</creator><general>Elsevier Inc</general><general>Elsevier BV</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20200315</creationdate><title>Novel antioxidant astaxanthin-s-allyl cysteine biconjugate diminished oxidative stress and mitochondrial dysfunction to triumph diabetes in rat model</title><author>Penislusshiyan, Sakayanathan ; 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AST-SAC (1 mg/kg/day) was treated against DM in rats for 45 days. The oxidative stress, antioxidants level, insulin secretion, activities of various carbohydrate metabolizing enzymes were studied. The glucose uptake in L6 myotubes was studied. In addition, in silico analysis of interaction of AST-SAC with proteins such as insulin receptor (IR) and 5′-adenosine monophosphate-activated protein kinase (AMPK) were carried out.
Administration of AST-SAC in DM rats has protected the mitochondrial function (decreased oxidative stress and normalized oxidative phosphorylation activities) and antioxidant capacity of the pancreas which has resulted in beta cells rejuvenation and insulin secretion restoration. AST-SAC decreased the alpha-glucosidases activities to bring glycemic control in DM rats. Due to these effects the glycoprotein components and lipids were restored to near normalcy in DM rats. AST-SAC protected the antioxidant status of liver, kidney and plasma; and curbed the progression of secondary complications of DM. AST-SAC treatment stimulated glucose uptake in L6 myotubes in in vitro. To support this observation, AST-SAC interacted with proteins such as IR and AMPK in silico.
AST-SAC can be considered as “multi-target-directed ligand”, that is, through these manifold effects, AST-SAC has been able to prevail over DM in rats.
[Display omitted]
•Astaxanthin-s-allyl cysteine biconjugate (AST-SAC) eased diabetes mellitus (DM).•AST-SAC improved overall as well as mitochondrial antioxidant status against DM.•AST-SAC protected the mitochondrial function against DM.•AST-SAC reduced small intestinal α-glucosidases activities against DM.•AST-SAC simulated glucose uptake in skeletal muscle cells.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>32001265</pmid><doi>10.1016/j.lfs.2020.117367</doi><tpages>11</tpages></addata></record> |
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| ispartof | Life sciences (1973), 2020-03, Vol.245, p.117367-11, Article 117367 |
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| subjects | Adenosine kinase Adenosine monophosphate AMP Animals Antidiabetes Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Astaxanthin Astaxanthin-s-allyl cysteine diester Beta cells Carbohydrates Cholesterol - metabolism Complications Cysteine Cysteine - analogs & derivatives Cysteine - pharmacology Cysteine - therapeutic use Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Glucose Glucose - metabolism Glycoproteins Hypoglycemic Agents - therapeutic use Insulin Insulin secretion Kidneys Kinases Lipids Male Mitochondria Mitochondria - drug effects Mitochondria - metabolism Molecular Docking Simulation Myotubes Oxidative phosphorylation Oxidative stress Oxidative Stress - drug effects Pancreas Phosphorylation Protein kinase Proteins Rats Rats, Sprague-Dawley Restoration Secretion Streptozocin Triglycerides - metabolism Xanthophylls - pharmacology Xanthophylls - therapeutic use |
| title | Novel antioxidant astaxanthin-s-allyl cysteine biconjugate diminished oxidative stress and mitochondrial dysfunction to triumph diabetes in rat model |
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