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Deep ocean minerals inhibit IL-6 and IGFIIR hypertrophic signalling pathways to attenuate diabetes-induced hypertrophy in rat hearts.

08:00 EDT 16th May 2019 | BioPortfolio

Summary of "Deep ocean minerals inhibit IL-6 and IGFIIR hypertrophic signalling pathways to attenuate diabetes-induced hypertrophy in rat hearts."

We previously reported that deep sea water (DSW) prolongs the life span of streptozotocin (STZ)-induced diabetic rats by the compensatory augmentation of the insulin like growth factor (IGF)-I survival signalling and inhibition of apoptosis. Here, we investigated the effects of DSW on cardiac hypertrophy in diabetic rats. Cardiac hypertrophy was induced in rats by using STZ (65 mg/kg) administered via IP injection. DSW was prepared by mixing DSW mineral extracts and desalinated water. Different dosages of DSW-1X (equivalent to 37 mg Mg/kg/day), 2X (equivalent to 74 mg Mg/kg/day) and 3X (equivalent to 111 mg Mg mg/kg/day) were administered to the rats through gavages for 4 weeks. Cardiac hypertrophy was evaluated by the heart weight to body weight ratio and the cardiac tissue cross-sectional area after haematoxylin and eosin staining. The protein levels of the cardiac hypertrophy signalling molecules were determined by Western blot. Our results showed that the suppressive effects of the DSW treatment on STZ-induced cardiac hypertrophy were comparable to those of MgSO administration and that the hypertrophic marker brain natriuretic peptide (BNP) was decreased by DSW. In addition, DSW attenuated both the eccentric hypertrophy signalling pathway, IL-6-MEK-STAT3, and the concentric signalling pathway, IGF-II-PKCa-CaMKII, in DM rat hearts. The cardiac hypertrophy associated activation of extracellular signal regulated kinase (ERK) and the upregulation of the transcription factor GATA binding protein 4 (GATA4) were also negated by treatment with DSW. The results from this study suggest that DSW could be a potential therapeutic agent for the prevention and treatment of diabetic cardiac hypertrophy.

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This article was published in the following journal.

Name: Journal of applied physiology (Bethesda, Md. : 1985)
ISSN: 1522-1601
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