Literature DB >> 34617183

Expression of Bax and Bcl-2 Proteins in Left-Ventricular Cardiomyocytes in Wistar-Kyoto and SHR Rats with Insulin-Dependent Diabetes Mellitus.

A P Sklifasovskaya1, M L Blagonravov2, A Yu Ryabinina1, M M Azova3, V A Goryachev1.   

Abstract

Loss of cardiomyocytes due to apoptotic or necrotic death is an important component of the pathogenesis of heart failure. Initiation of apoptosis by the mitochondrial pathway depends on the balance between proapoptotic and antiapoptotic factors, in particular, Bax and Bcl-2. Cardiomyocyte apoptosis in essential hypertension is studied in sufficient details. At the same time, apoptotic processes in the myocardium in diabetes mellitus alone and in combination with essential hypertension remain poorly understood. Here we studied the expression of Bax and Bcl-2 in the left ventricular cardiomyocytes of 38-week-old male Wistar-Kyoto rats and 38- and 57-week-old SHR rats with essential hypertension, diabetes mellitus, and a combination of these pathologies. Insulin-dependent diabetes mellitus was modelled by a single parenteral administration of streptozotocin in a dose 65 mg/kg. Expression of Bax and Bcl-2 was assessed by the immunohistochemical method. In essential hypertension and diabetes mellitus, the apoptotic processes in the ventricular myocardium were enhanced, as is seen from the increase in the content of the proapoptotic factor Bax and a decrease in the expression of the antiapoptotic factor Bcl-2. However, in case of combined pathology, Bax content increased less markedly, while the expression of antiapoptotic Bcl-2 was significantly increased.
© 2021. Springer Science+Business Media, LLC, part of Springer Nature.

Entities:  

Keywords:  Bax; Bcl-2; diabetes mellitus; essential hypertension; myocardium

Mesh:

Substances:

Year:  2021        PMID: 34617183     DOI: 10.1007/s10517-021-05272-7

Source DB:  PubMed          Journal:  Bull Exp Biol Med        ISSN: 0007-4888            Impact factor:   0.804


  13 in total

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Review 10.  Regulating microRNA expression: at the heart of diabetes mellitus and the mitochondrion.

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