The aim of the present study was to explore whether the hypertrophy of H9C2 cardiomyocytes was induced by high glucose, to investigate whether the calcium channel inhibitor (Norvasc) could inhibit this process and to clarify the possible signaling pathways. The morphology of H9C2 cells was observed under an optical microscope, and the cell surface area was measured by Image Pro Plus 6.1 software. Furthermore, fluorescence spectrophotometry was used to detect intracellular calcium concentration ([Ca 2+ ]i). ELISA was performed to detect calcineurin (CaN) activity; reverse transcription-quantitative PCR and western blotting were performed to detect the mRNA and protein expression levels of CaN Aβ subunit (CnAβ), nuclear factor of activated T cells 3 (NFAT3) and β type myosin heavy chain (β-MHC). Cell size was increased with the increase in glucose concentration of culture medium at 48 and 72 h, respectively, and decreased with the addition of Norvasc compared with those without Norvasc (P<0.05). There was no significant difference in cell size with the addition of Norvasc compared with cells cultured with 5 mM glucose (P>0.05). The average [Ca 2+ ]i activity of single cells in the 48- and 72-h culture groups treated with 50 mM glucose was significantly higher than cells treated with 5 mM glucose (P<0.05); and the fluorescent value of average [Ca 2+ ]i activity of single cells was lower, following the addition of Norvasc than that without Norvasc (P<0.05). CaN activity in the 48- and 72-h culture group treated with 50 mM glucose was markedly higher than that treated with 5 mM glucose, and the activity of CaN notably decreased with the addition of Norvasc compared with those without Norvasc. The mRNA and protein expression levels of CnAβ, NFAT3 and β-MHC in the 48- and 72-h culture groups treated with 50 mM glucose were all significantly higher than those treated with 5 mM glucose (P<0.05). The mRNA and protein expression of CnAβ, NFAT3 and β-MHC cultured with 50 mM glucose were significantly decreased following the addition of Norvasc (P<0.05). Thus, the calcium channel inhibitor Norvasc may inhibit high glucose-induced hypertrophy of H9C2 cardiomyocytes by inhibiting the Ca 2+ -CaN-NFAT3 signaling pathway.

Lung cancer shows a high rate of incidence and mortality. This study aimed to investigate the influence of octreotide (OCT) on lipopolysaccharide (LPS)-induced apoptosis and metabolome expression in A549 cells. After A549 cells were treated by LPS or co-cultured with LPS and OCT, cell apoptosis was tested by flow cytometry, and gas chromatography-mass spectrometer (GC/MS) and high-performance liquid chromatography-mass spectrometer (LC/MS) were subjected to determine the differently expressed metabolites, and the interaction network was constructed. Results found that OCT promoted the apoptosis of A549 cells and significantly affected LPS-regulated cell apoptosis. Following the further investigation by orthogonal partial least squares discriminant analysis (OPLS-DA), the metabolites with different expression levels were obtained, and most of which belong to amino acids, phospholipids, organic acid, and saccharides. Fourteen components with the role of the marker metabolites included serotonin, indole, threonine, serine, glucose, phenylalanine, lactose, fumarate, 4-hydroxyphenyllactate, aspartate, asparagine, putrescine, proline, and succinate. It is indicated that OCT promotes apoptosis through five metabolism pathways and 14 key metabolism elements in A549 cells.