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Acta Medica Iranica، جلد ۶۰، شماره ۱، صفحات ۴۰-۴۵

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عنوان انگلیسی FPS-ZM1 Alleviates Circulating Indices of Liver Injury in Diet-Induced Type 2 Diabetic Mice
چکیده انگلیسی مقاله Despite dietary/lifestyle modifications as well as glycemic and lipid control, non-alcoholic fatty liver disease (NAFLD) imposes a considerable risk to the patients by advancing to non-alcoholic steatohepatitis (NASH). The present investigation aims to evaluate the protective potential of FPS-ZM1, a selective inhibitor for advanced glycation end products (RAGE), against circulating indices of liver injury in high fat diet-induced diabetic mice. FPS-ZM1 at 0.5. 1, and 2 mg/kg (orally) was administered for 2 months, starting 4 months after provision of the high-fat diet. Tests for glucose homeostasis, liver injury markers, and hepatic/plasma miR-21 expressions were performed. FPS-ZM1 attenuated diabetes-induced elevations in serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glutamate dehydrogenase (GLD), and alpha glutathione-S-transferase (α-GST) as well as alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT). It also decreased diabetes-associated elevations in serum ferritin and plasma cytokeratin 18 fragments. Additionally, FPS-ZM1 down-regulated elevated expressions of miR-21 in the liver and plasma of diabetic mice. These findings highlight the benefits of FPS-ZM in alleviating liver injury in mice evoked by high-fat diet-induced type 2 diabetes and suggest FPS-ZM1 as a new potential adjunct to the conventional diet/lifestyle modification and glycemic control in diabetics.
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نویسندگان مقاله | Somayeh Aslani
Department of Biochemistry, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran


| Saman Bahrambeigi
Department of Basic Sciences, School of Veterinary Medicine, Urmia University, Urmia, Iran


| Davoud Sanajou
Department of Biochemistry, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran



نشانی اینترنتی https://acta.tums.ac.ir/index.php/acta/article/view/8669
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