Calcium inhibitor inhibits high glucose‑induced hypertrophy of H9C2 cells.

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 ([Ca2+]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 [Ca2+]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 [Ca2+]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 Ca2+‑CaN‑NFAT3 signaling pathway.