Fig. 2

Intracellular Ca²⁺ signaling in empagliflozin-treated atrial fibroblasts. A Representative intracellular Ca²⁺ tracing from control (left upper panels), and empagliflozin (1 μmol/L, right upper panels)-treated atrial fibroblasts. Where indicated, thapsigargin was added to the calcium-free buffer to induce ER Ca²⁺ depletion. After the intracellular Ca²⁺ surge induced by thapsigargin (ER calcium) was returned to the steady state, the extracellular Ca²⁺ concentration was then increased to 2 mmol/L to measure Ca²⁺ entry. F₃₄₀/F₃₈₀ was expressed as the relative intracellular Ca²⁺. The left lower panel displays the change (∆ F₃₄₀/F₃₈₀) of Ca²⁺ measured by area under curve of Ca²⁺ tracing (AUC, statistic test by unpaired t-test), the change from baseline to peak calcium amplitude (statistic test by Mann–Whitney Rank Sum Test), and the decay time of Ca²⁺ entry (T50, calculated from the peak to the 50% of the decay or the end of the calcium image recording, statistic test by unpaired t-test) in control (n = 5) and empagliflozin-treated atrial fibroblasts (n = 5). B Averaged data of the levels of IP3 in the control cells and fibroblasts treated with empagliflozin (1 μmol/L) for 48 h (n = 6 experiments, statistic test by pair t-test). C Photographs and averaged data of the expression of phosphorylated phospholipase C (pPLC) in the control cells and fibroblasts treated with empagliflozin (1 μmol/L) for 48 h (n = 6 independent experiments, statistic test by paired t-test). GAPDH was used as a loading control. * p < 0.05, ^# p < 0.01, ^$ p < 0.005