PubMed:24842192 JSONTXT

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T1","span":{"begin":558,"end":562},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:10118"},{"id":"A2","pred":"db_id","subj":"T1","obj":"NCBItxid:10116"},{"id":"A3","pred":"db_id","subj":"T1","obj":"NCBItxid:10114"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":151},"obj":"Sentence"},{"id":"T2","span":{"begin":152,"end":330},"obj":"Sentence"},{"id":"T3","span":{"begin":331,"end":545},"obj":"Sentence"},{"id":"T4","span":{"begin":546,"end":759},"obj":"Sentence"},{"id":"T5","span":{"begin":760,"end":877},"obj":"Sentence"},{"id":"T6","span":{"begin":878,"end":1009},"obj":"Sentence"},{"id":"T7","span":{"begin":1010,"end":1122},"obj":"Sentence"},{"id":"T8","span":{"begin":1123,"end":1337},"obj":"Sentence"},{"id":"T9","span":{"begin":1338,"end":1407},"obj":"Sentence"},{"id":"T10","span":{"begin":1408,"end":1485},"obj":"Sentence"},{"id":"T11","span":{"begin":1486,"end":1627},"obj":"Sentence"},{"id":"T12","span":{"begin":1628,"end":1806},"obj":"Sentence"},{"id":"T13","span":{"begin":1807,"end":1884},"obj":"Sentence"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

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treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":129,"end":150},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":210,"end":231},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":480,"end":501},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":849,"end":876},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":855,"end":876},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1678,"end":1699},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005068"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005068"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005068"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0004781"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005068"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005068"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

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{"project":"LitCoin-GeneOrGeneProduct-v2","denotations":[{"id":"T1","span":{"begin":44,"end":64},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":294,"end":322},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":324,"end":328},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":431,"end":451},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":453,"end":457},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":526,"end":530},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":1199,"end":1203},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":1204,"end":1208},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":1234,"end":1241},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1246,"end":1251},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1254,"end":1281},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":1295,"end":1308},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":1310,"end":1314},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1323,"end":1328},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1338,"end":1345},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1402,"end":1406},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":1501,"end":1505},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1510,"end":1514},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1673,"end":1677},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1790,"end":1794},"obj":"GeneOrGeneProduct"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":90,"end":118},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":129,"end":150},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":210,"end":231},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":250,"end":262},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":407,"end":426},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":480,"end":501},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":855,"end":876},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1014,"end":1042},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1254,"end":1259},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1260,"end":1268},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1678,"end":1699},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1700,"end":1719},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1735,"end":1747},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T14","span":{"begin":1863,"end":1872},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A10","pred":"originalLabel","subj":"T10","obj":"D009336"},{"id":"A5","pred":"originalLabel","subj":"T5","obj":"DISEASE"},{"id":"A1","pred":"originalLabel","subj":"T1","obj":"D018487"},{"id":"A3","pred":"originalLabel","subj":"T3","obj":"D009203"},{"id":"A14","pred":"originalLabel","subj":"T14","obj":"D007238"},{"id":"A6","pred":"originalLabel","subj":"T6","obj":"D009203"},{"id":"A11","pred":"originalLabel","subj":"T11","obj":"D009203"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"D009203"},{"id":"A7","pred":"originalLabel","subj":"T7","obj":"D009203"},{"id":"A8","pred":"originalLabel","subj":"T8","obj":"D018487"},{"id":"A4","pred":"originalLabel","subj":"T4","obj":"DISEASE"},{"id":"A13","pred":"originalLabel","subj":"T13","obj":"DISEASE"},{"id":"A12","pred":"originalLabel","subj":"T12","obj":"DISEASE"},{"id":"A9","pred":"originalLabel","subj":"T9","obj":"D009369"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":44,"end":64},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":294,"end":322},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":324,"end":328},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":431,"end":451},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":453,"end":457},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":526,"end":530},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":1199,"end":1203},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":1246,"end":1251},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":1254,"end":1281},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1295,"end":1308},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1310,"end":1314},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":1402,"end":1406},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":1501,"end":1505},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":1510,"end":1514},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":1790,"end":1794},"obj":"GeneOrGeneProduct"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":129,"end":150},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":210,"end":231},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":480,"end":501},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":849,"end":876},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":1254,"end":1259},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1678,"end":1699},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1822,"end":1825},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005068"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005068"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0004781"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0005070"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0005068"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005068"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0012833"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":90,"end":118},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":129,"end":150},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":210,"end":231},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":250,"end":262},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":407,"end":426},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":480,"end":501},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":855,"end":876},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1014,"end":1042},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1254,"end":1259},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1260,"end":1268},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":1678,"end":1699},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":1700,"end":1719},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T13","span":{"begin":1735,"end":1747},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A6","pred":"ID:","subj":"T6","obj":"D009203"},{"id":"A9","pred":"ID:","subj":"T9","obj":"D009369"},{"id":"A13","pred":"ID:","subj":"T13","obj":"DISEASE"},{"id":"A10","pred":"ID:","subj":"T10","obj":"D009336"},{"id":"A8","pred":"ID:","subj":"T8","obj":"D018487"},{"id":"A4","pred":"ID:","subj":"T4","obj":"DISEASE"},{"id":"A7","pred":"ID:","subj":"T7","obj":"D009203"},{"id":"A11","pred":"ID:","subj":"T11","obj":"D009203"},{"id":"A12","pred":"ID:","subj":"T12","obj":"DISEASE"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D018487"},{"id":"A3","pred":"ID:","subj":"T3","obj":"D009203"},{"id":"A5","pred":"ID:","subj":"T5","obj":"DISEASE"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D009203"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":90,"end":118},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":129,"end":150},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":210,"end":231},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":407,"end":426},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":480,"end":501},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":855,"end":876},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1014,"end":1042},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1254,"end":1259},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":1678,"end":1699},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":1700,"end":1719},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A3","pred":"#label","subj":"T3","obj":"D009203"},{"id":"A10","pred":"#label","subj":"T10","obj":"DISEASE"},{"id":"A6","pred":"#label","subj":"T6","obj":"D009203"},{"id":"A7","pred":"#label","subj":"T7","obj":"D018487"},{"id":"A1","pred":"#label","subj":"T1","obj":"D018487"},{"id":"A2","pred":"#label","subj":"T2","obj":"D009203"},{"id":"A4","pred":"#label","subj":"T4","obj":"DISEASE"},{"id":"A5","pred":"#label","subj":"T5","obj":"D009203"},{"id":"A8","pred":"#label","subj":"T8","obj":"D009369"},{"id":"A9","pred":"#label","subj":"T9","obj":"D009203"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":558,"end":562},"obj":"OrganismTaxon"}],"text":"Chronic treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. Metfromin markedly lowered isoproterenol-induced elevation in the levels of TLR4 mRNA, myeloid differentiation protein 88 (MyD88), tumor necrosis factor-alpha (TNF-α), and interleukin 6 (IL-6) in the heart tissues. Similar changes were also seen in the serum levels of TNF-α and IL-6. However, the lower doses of 25 and 50mg/kg were more effective than 100mg/kg. Phosphorylated AMPKα (p-AMPK) in the myocardium was significantly elevated by 25mg/kg of metformin, slightly by 50mg/kg, but not by 100mg/kg. Chronic pre-treatment with metformin reduces post-myocardial infarction cardiac dysfunction and suppresses inflammatory responses, possibly through inhibition of TLR4 activities. This mechanism can be considered as a target to protect infarcted myocardium."}

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treatment with metformin suppresses toll-like receptor 4 signaling and attenuates left ventricular dysfunction following myocardial infarction.\nAcute treatment with metformin has a protective effect in myocardial infarction by suppression of inflammatory responses due to activation of AMP-activated protein kinase (AMPK). In the present study, the effect of chronic pre-treatment with metformin on cardiac dysfunction and toll-like receptor 4 (TLR4) activities following myocardial infarction and their relation with AMPK were assessed. Male Wistar rats were randomly assigned to one of 5 groups (n=6): normal control and groups were injected isoproterenol after chronic pre-treatment with 0, 25, 50, or 100mg/kg of metformin twice daily for 14 days. Isoproterenol (100mg/kg) was injected subcutaneously on the 13th and 14th days to induce acute myocardial infarction. Isoproterenol alone decreased left ventricular systolic pressure and myocardial contractility indexed as LVdp/dtmax and LVdp/dtmin. The left ventricular dysfunction was significantly lower in the groups treated with 25 and 50mg/kg of metformin. 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