Ruisha Li,Keyin Zhang,Zhenjun Xu,Yanrong Yu,Dongjin Wang,Kai Li,Wenxue Liu,Jun Pan
Recent studies have underscored the cardioprotective properties of liraglutide. This research explores its impact on cardiac hypertrophy and heart failure following transverse aortic constriction (TAC). We found that liraglutide administration markedly ameliorated cardiac hypertrophy, fibrosis, and function. These benefits correlated with increased ANP expression and reduced activity in the calcineurin A/NFATc3 signaling pathway. Moreover, liraglutide mitigated ER stress and cardiomyocyte apoptosis, and enhanced autophagy. Notably, the positive effects of liraglutide diminished when co-administered with A71915, an ANP inhibitor, suggesting that ANP upregulation is critical to its cardioprotective mechanism.
The method of nanofluid flooding to enhance heavy oil recovery has attracted much attention in oilfields. An EOR technology named alkali - silica nanoparticle-polymer (ANP) flooding was designed to enhance heavy oil recovery. The performance of the ANP flood system on reducing interfacial tension (IFT), altering the wettability of rock surface, emulsifying and displacing heavy oil were compared with that of polymer (P), alkali - polymer (AP) and nanoparticle - polymer (NP) flood systems. Visual flooding test was conducted to investigate the displacement mechanisms of different flood systems in porous media . ANP nanofluid could remain stable over 30 days without sedimentation of nanoparticles. The emulsifying ability of the four flood systems for heavy oil followed the order: P < NP < AP < ANP. Based on the analysis of droplet size distribution of emulsion and changes of IFT value with alkali concentration, the best formula of ANP system to emulsify heavy oil was 0.3% [w/v] Na 2 CO 3 + 0.1% [w/v] silica nanoparticle + 1000 mg L −1 polymer. Electrostatic repulsion between silica nanoparticles and oil droplets played a dominated role on stabling ANP emulsion. ANP flood system could change the wettability of rock surface to a more water-wet state (contact angle varied from 85.4° to 35.6°). Core and visual flooding tests proved that ANP flood system had a better sweep and displacement efficiency for heavy oil than other three flood systems (P, AP and NP), which could enhance heavy oil recovery by 21.19% after water flooding in a sandstone core. Emulsification is the main mechanism for ANP flooding to enhance heavy oil recovery.
Wentao Sun,Yang Zhou,Hongmei Xue,Haitao Hou,Guowei He,Qin Yang
Although the association of elevated homocysteine level with cardiac hypertrophy has been reported, the molecular mechanisms by which homocysteine induces cardiac hypertrophy remain inadequately understood. In this study we aim to uncover the roles of cyclic nucleotide phosphodiesterase 1 (PDE1) and endoplasmic reticulum (ER) stress and their relationship to advance the mechanistic understanding of homocysteine-induced cardiac cell hypertrophy. H9c2 cells and primary neonatal rat cardiomyocytes are exposed to homocysteine with or without ER stress inhibitor TUDCA or PDE1-specific inhibitor Lu AF58027, or transfected with siRNAs targeting PDE1 isoforms prior to homocysteine-exposure. Cell surface area is measured and ultrastructure is examined by transmission electron microscopy. Hypertrophic markers, PDE1 isoforms, and ER stress molecules are detected by q-PCR and western blot analysis. Intracellular cGMP and cAMP are measured by ELISA. The results show that homocysteine causes the enlargement of H9c2 cells, increases the expressions of hypertrophic markers β-MHC and ANP, upregulates PDE1A and PDE1C, promotes the expressions of ER stress molecules, and causes ER dilatation and degranulation. TUDCA and Lu AF58027 downregulate β-MHC and ANP, and alleviate cell enlargement. TUDCA decreases PDE1A and PDE1C levels. Silencing of PDE1C inhibits homocysteine-induced hypertrophy, whereas PDE1A knockdown has minor effect. Both cAMP and cGMP are decreased after homocysteine-exposure, while only cAMP is restored by Lu AF58027 and TUDCA. TUDCA and Lu AF58027 also inhibit cell enlargement, downregulate ANP, β-MHC and PDE1C, and enhance cAMP level in homocysteine-exposed primary cardiomyocytes. ER stress mediates homocysteine-induced hypertrophy of cardiac cells via upregulating PDE1C expression Cyclic nucleotide, especially cAMP, is the downstream mediator of the ER stress-PDE1C signaling axis in homocysteine-induced cell hypertrophy.
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