Peculiarities of the antiapoptotic Bcl-2 protein expression in liver in a model of obesity and type 2 diabetes and with linaglyptin correction
Background. XXI century is known as a century of obesity and type 2 diabetes (T2D), one of the main reasons of nonalcoholic fatty liver disease (NAFLD). Severe forms of NAFLD, such as non-alcoholic steatohepatitis and cirrhosis, are associated with process of apoptosis. A great contributor in the de...
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| Formato: | article |
| Lenguaje: | RU |
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Scientific Сentre for Family Health and Human Reproduction Problems
2018
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| Acceso en línea: | https://doaj.org/article/885df33e57d1482cb29c0868ac9d9967 |
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| Sumario: | Background. XXI century is known as a century of obesity and type 2 diabetes (T2D), one of the main reasons of nonalcoholic fatty liver disease (NAFLD). Severe forms of NAFLD, such as non-alcoholic steatohepatitis and cirrhosis, are associated with process of apoptosis. A great contributor in the developing of NAFLD is a dysfunction of hematolymphatic barrier and linagliptin showed positive effect on this. The group of inhibitors of apoptosis - Bcl-2 resists to wide variety of pro-apoptotic proteins. Studying correction of apoptosis can be the key to the treatment of NAFLD, and that is a reason of high interest in anti-apoptotic Bcl-2 protein. Aims. To assess the features of the expression of the anti-apoptotic Bcl-2 protein in the liver of db/db mice in the model of obesity and type 2 diabetes mellitus and with linaglyptin correction. Materials and methods. Experiment was performed on type 11 (db/db) diabetic mice. Linaglyptin or placebo was administered daily by gavage from the 8th to 16th weeks of life. Results. The week immunohistochemical reaction for antiapoptotic protein Bcl-2 was found in placebo-treated mice. Whereas treatment with Linaglyptin shifted the ratio of apoptosis regulators following significant increase in the area of Bcl-2 expression. Conclusions. The obtained results demonstrate a "try" at antiapoptotic activity of the Linaglyptin in the liver in the model of T2D. |
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