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Wilma Helena De Oliveira - One of the best experts on this subject based on the ideXlab platform.
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effects of the new Thiazolidine Derivative lpsf gq 02 on hepatic lipid metabolism pathways in non alcoholic fatty liver disease nafld
European Journal of Pharmacology, 2016Co-Authors: Shyrlene Meiry Da Rocha Araujo, Amanda Karolina Soares E Silva, Fabiana Oliveira Dos Santos Gomes, Edlene Lima Ribeiro, Wilma Helena De OliveiraAbstract:Abstract Non-alcoholic fatty liver disease (NAFLD) is considered the most common manifestation of metabolic syndrome. One of its most important features is the accumulation of triglycerides in the hepatocyte cells. Thiazolidinediones (TZDs) act as insulin sensitizers and are used to treat patients with type 2 diabetes and other conditions that are resistant to insulin, such as hepatic steatosis. Controversially, TZDs are also associated with the development of cardiovascular events and liver problems. For this reason, new therapeutic strategies are necessary to improve liver function in patients with chronic liver diseases. The aim of the present study was to evaluate the effects of LPSF/GQ-02 on the liver lipid metabolism in a murine model of NAFLD. Eighty male LDLR-/- mice were divided into 3 groups: 1–fed with a high-fat diet (HFD); 2–HFD+Pioglitazone (20 mg/kg/day); 3–HFD+LPSF/GQ-02 (30 mg/kg/day). The experiments lasted 12 weeks and drugs were administered daily by gavage in the final four weeks. The liver was processed for optical microscopy, Oil Red O, immunohistochemistry, immunofluorescence and western blot analysis. LPSF/GQ-02 effectively decreased fat accumulation, increased the hepatic levels of p-AMPK, FoxO1, ATGL, p-ACC and PPARα, and reduced the expression of LXRα, SREBP-1c and ACC. These results suggest that LPSF/GQ-02 acts directly on the hepatic lipid metabolism through the activation of the PPAR-α/AMPK/FoxO1/ATGL lipolytic pathway, and the inhibition of the AMPK/LXR/SREBP-1c/ACC/FAS lipogenic pathway.
Fabiana Oliveira Dos Santos Gomes - One of the best experts on this subject based on the ideXlab platform.
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effects of the new Thiazolidine Derivative lpsf gq 02 on hepatic lipid metabolism pathways in non alcoholic fatty liver disease nafld
European Journal of Pharmacology, 2016Co-Authors: Shyrlene Meiry Da Rocha Araujo, Amanda Karolina Soares E Silva, Fabiana Oliveira Dos Santos Gomes, Edlene Lima Ribeiro, Wilma Helena De OliveiraAbstract:Abstract Non-alcoholic fatty liver disease (NAFLD) is considered the most common manifestation of metabolic syndrome. One of its most important features is the accumulation of triglycerides in the hepatocyte cells. Thiazolidinediones (TZDs) act as insulin sensitizers and are used to treat patients with type 2 diabetes and other conditions that are resistant to insulin, such as hepatic steatosis. Controversially, TZDs are also associated with the development of cardiovascular events and liver problems. For this reason, new therapeutic strategies are necessary to improve liver function in patients with chronic liver diseases. The aim of the present study was to evaluate the effects of LPSF/GQ-02 on the liver lipid metabolism in a murine model of NAFLD. Eighty male LDLR-/- mice were divided into 3 groups: 1–fed with a high-fat diet (HFD); 2–HFD+Pioglitazone (20 mg/kg/day); 3–HFD+LPSF/GQ-02 (30 mg/kg/day). The experiments lasted 12 weeks and drugs were administered daily by gavage in the final four weeks. The liver was processed for optical microscopy, Oil Red O, immunohistochemistry, immunofluorescence and western blot analysis. LPSF/GQ-02 effectively decreased fat accumulation, increased the hepatic levels of p-AMPK, FoxO1, ATGL, p-ACC and PPARα, and reduced the expression of LXRα, SREBP-1c and ACC. These results suggest that LPSF/GQ-02 acts directly on the hepatic lipid metabolism through the activation of the PPAR-α/AMPK/FoxO1/ATGL lipolytic pathway, and the inhibition of the AMPK/LXR/SREBP-1c/ACC/FAS lipogenic pathway.
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Effect of new Thiazolidine Derivatives LPSF/GQ-02 and LPSF/GQ-16 on atherosclerotic lesions in LDL receptor-deficient mice (LDLR−/−)
Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology, 2012Co-Authors: Amanda Karolina Soares E Silva, Fabiana Oliveira Dos Santos Gomes, Dilênia De Oliveira Cipriano Torres, Sura Wanessa Santos Rocha, Bruna Dos Santos Silva, M.a.m. Donato, Catarina Rapôso, Ana Célia Oliveira Dos Santos, Maria Do Carmo Alves De Lima, Suely Lins GaldinoAbstract:Abstract Background Atherosclerotic cardiovascular disease is a chronic inflammatory condition. Thiazolidinediones (TZDs) are used to enhance sensitivity to insulin and have demonstrated a protective effect over a variety of cardiovascular markers and risk factors. Controversially, the TZDs are associated with the development of heart failure. Thus, lines of research have invested in the search for new molecules in order to obtain more selective and less harmful treatment alternatives for the pathogenesis of atherosclerosis and its risk factors. Methods Animals were fed a diet rich in fat for 10 weeks. In the last 2 weeks, animals received either pioglitazone, LPSF/GQ-02, or LPSF/GQ-16 daily through gavage. At the end of the treatment, blood was collected for biochemical analysis and the aortas were dissected for subsequent analyses. Results No changes in the blood lipid profile were found following the use of the drugs in comparison to the control. However, the new Thiazolidine Derivatives were more efficient in improving insulin resistance in comparison to pioglitazone and the control group. Morphometric analyses revealed that neither pioglitazone nor LPSF/GQ16 led to satisfactory effects over atherosclerosis. However, LPSF/GQ-02 led to a reduction in area of the atherosclerotic lesions. Ultrastructural analyses revealed extensive degeneration of the endothelium and an increase in apoptotic cells in the subendothelial space following the use of pioglitazone and LPSF/GQ-16. However, LPSF/GQ-02 caused minimal cell alterations in the aortic endothelium. Regarding markers, endothelial nitric oxide synthase (eNOS) and matrix metalloproteinase 9 (MMP-9), LPSF/GQ-16, and pioglitazone exerted similar effects, increasing the expression of MMP-9, and had no effect on the expression of eNOS compared with the control group. On the other hand, LPSF/GQ-02 was effective in reducing the expression of MMP-9 and increased eNOS significantly. Conclusions The results suggest that the new Thiazolidine Derivative LPSF/GQ-02 is a promising candidate for the treatment of atherosclerosis.
Shyrlene Meiry Da Rocha Araujo - One of the best experts on this subject based on the ideXlab platform.
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effects of the new Thiazolidine Derivative lpsf gq 02 on hepatic lipid metabolism pathways in non alcoholic fatty liver disease nafld
European Journal of Pharmacology, 2016Co-Authors: Shyrlene Meiry Da Rocha Araujo, Amanda Karolina Soares E Silva, Fabiana Oliveira Dos Santos Gomes, Edlene Lima Ribeiro, Wilma Helena De OliveiraAbstract:Abstract Non-alcoholic fatty liver disease (NAFLD) is considered the most common manifestation of metabolic syndrome. One of its most important features is the accumulation of triglycerides in the hepatocyte cells. Thiazolidinediones (TZDs) act as insulin sensitizers and are used to treat patients with type 2 diabetes and other conditions that are resistant to insulin, such as hepatic steatosis. Controversially, TZDs are also associated with the development of cardiovascular events and liver problems. For this reason, new therapeutic strategies are necessary to improve liver function in patients with chronic liver diseases. The aim of the present study was to evaluate the effects of LPSF/GQ-02 on the liver lipid metabolism in a murine model of NAFLD. Eighty male LDLR-/- mice were divided into 3 groups: 1–fed with a high-fat diet (HFD); 2–HFD+Pioglitazone (20 mg/kg/day); 3–HFD+LPSF/GQ-02 (30 mg/kg/day). The experiments lasted 12 weeks and drugs were administered daily by gavage in the final four weeks. The liver was processed for optical microscopy, Oil Red O, immunohistochemistry, immunofluorescence and western blot analysis. LPSF/GQ-02 effectively decreased fat accumulation, increased the hepatic levels of p-AMPK, FoxO1, ATGL, p-ACC and PPARα, and reduced the expression of LXRα, SREBP-1c and ACC. These results suggest that LPSF/GQ-02 acts directly on the hepatic lipid metabolism through the activation of the PPAR-α/AMPK/FoxO1/ATGL lipolytic pathway, and the inhibition of the AMPK/LXR/SREBP-1c/ACC/FAS lipogenic pathway.
Edlene Lima Ribeiro - One of the best experts on this subject based on the ideXlab platform.
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effects of the new Thiazolidine Derivative lpsf gq 02 on hepatic lipid metabolism pathways in non alcoholic fatty liver disease nafld
European Journal of Pharmacology, 2016Co-Authors: Shyrlene Meiry Da Rocha Araujo, Amanda Karolina Soares E Silva, Fabiana Oliveira Dos Santos Gomes, Edlene Lima Ribeiro, Wilma Helena De OliveiraAbstract:Abstract Non-alcoholic fatty liver disease (NAFLD) is considered the most common manifestation of metabolic syndrome. One of its most important features is the accumulation of triglycerides in the hepatocyte cells. Thiazolidinediones (TZDs) act as insulin sensitizers and are used to treat patients with type 2 diabetes and other conditions that are resistant to insulin, such as hepatic steatosis. Controversially, TZDs are also associated with the development of cardiovascular events and liver problems. For this reason, new therapeutic strategies are necessary to improve liver function in patients with chronic liver diseases. The aim of the present study was to evaluate the effects of LPSF/GQ-02 on the liver lipid metabolism in a murine model of NAFLD. Eighty male LDLR-/- mice were divided into 3 groups: 1–fed with a high-fat diet (HFD); 2–HFD+Pioglitazone (20 mg/kg/day); 3–HFD+LPSF/GQ-02 (30 mg/kg/day). The experiments lasted 12 weeks and drugs were administered daily by gavage in the final four weeks. The liver was processed for optical microscopy, Oil Red O, immunohistochemistry, immunofluorescence and western blot analysis. LPSF/GQ-02 effectively decreased fat accumulation, increased the hepatic levels of p-AMPK, FoxO1, ATGL, p-ACC and PPARα, and reduced the expression of LXRα, SREBP-1c and ACC. These results suggest that LPSF/GQ-02 acts directly on the hepatic lipid metabolism through the activation of the PPAR-α/AMPK/FoxO1/ATGL lipolytic pathway, and the inhibition of the AMPK/LXR/SREBP-1c/ACC/FAS lipogenic pathway.
Amanda Karolina Soares E Silva - One of the best experts on this subject based on the ideXlab platform.
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effects of the new Thiazolidine Derivative lpsf gq 02 on hepatic lipid metabolism pathways in non alcoholic fatty liver disease nafld
European Journal of Pharmacology, 2016Co-Authors: Shyrlene Meiry Da Rocha Araujo, Amanda Karolina Soares E Silva, Fabiana Oliveira Dos Santos Gomes, Edlene Lima Ribeiro, Wilma Helena De OliveiraAbstract:Abstract Non-alcoholic fatty liver disease (NAFLD) is considered the most common manifestation of metabolic syndrome. One of its most important features is the accumulation of triglycerides in the hepatocyte cells. Thiazolidinediones (TZDs) act as insulin sensitizers and are used to treat patients with type 2 diabetes and other conditions that are resistant to insulin, such as hepatic steatosis. Controversially, TZDs are also associated with the development of cardiovascular events and liver problems. For this reason, new therapeutic strategies are necessary to improve liver function in patients with chronic liver diseases. The aim of the present study was to evaluate the effects of LPSF/GQ-02 on the liver lipid metabolism in a murine model of NAFLD. Eighty male LDLR-/- mice were divided into 3 groups: 1–fed with a high-fat diet (HFD); 2–HFD+Pioglitazone (20 mg/kg/day); 3–HFD+LPSF/GQ-02 (30 mg/kg/day). The experiments lasted 12 weeks and drugs were administered daily by gavage in the final four weeks. The liver was processed for optical microscopy, Oil Red O, immunohistochemistry, immunofluorescence and western blot analysis. LPSF/GQ-02 effectively decreased fat accumulation, increased the hepatic levels of p-AMPK, FoxO1, ATGL, p-ACC and PPARα, and reduced the expression of LXRα, SREBP-1c and ACC. These results suggest that LPSF/GQ-02 acts directly on the hepatic lipid metabolism through the activation of the PPAR-α/AMPK/FoxO1/ATGL lipolytic pathway, and the inhibition of the AMPK/LXR/SREBP-1c/ACC/FAS lipogenic pathway.